HETEROTROPHIC NUTRITION

This is the type of nutrition in which organisms take in ready made organic food substances made by autotrophs (producers).

TYPES OF HETEROTROPHIC NUTRITION

(a) Holozoic nutrition
(b) Saprotrophic nutrition (Saprophytic nutrition)
(c) Symbiosis: (i) Parasitism (ii) Mutualism (iii) Commensalism

HOLOZOIC NUTRITION
This is the type of nutrition in which complex organic food is taken in and broken down inside the body of an organism into
simple soluble molecules which are then absorbed and assimilated.

BASIC PROCESSES INVOLVED IN HOLOZOIC NUTRITION

1. Obtaining food: May involve movements to capture or find new food sources from the environment.
2. Ingestion: The intake of food into the body (feeding mechanisms).

3. Digestion: Chemical breakdown (by enzymes) and physical breakdown (by teeth, gizzard, mandibles, radula)
of large insoluble molecules of food into small soluble molecules.

4. Absorption: The uptake of nutrient molecules into the cells of the digestive tract and, from there, into the bloodstream
5. Defecation (Egestion): elimination of undigested residue.
6. Assimilation: The utilization of the absorbed soluble food substances to form energy or materials which are
incorporated into the body tissues.

FEEDING MECHANISMS OF ANIMALS

Nature of Mechanism Organisms Description
food

filter feeding / Whales, sharks, flamingo, Body appendages (gills/beaks/keratinous plates) filter
microphagous herring; planktons/blue green algae suspended in water into body

feeding; cavity /mouth then digestion occurs.

Pseudopodia enclose the food particle to form food

vacuoles which on associating with primary lysosomes
form secondary lysosomes, and after digestion, soluble
Pseudopodial products simply/facilitatively diffuse /actively move into
Amoeba the cytoplasm while undigested wastes are egested by
feeding
exocytosis.

Flagellate feeding Euglena, sponges Flagellar beating directs microscopic food particles to the
region of ingestion, then intracellular digestion occurs.
Small
Ciliary feeding Paramecium, Amphioxus Cilia beating directs microscopic food particles to the
particles
 region of ingestion, then intracellular digestion occurs.
Tentacular Sea cucumber Mucus on tentacles traps food particles
feeding

Setous feeding Water flea (Daphnia), culex Setae on appendages trap and direct small food particles
mosquito larvae into the digestive system.

Mucoid feeding Some molluscs Mucus layer traps food particles, later swallowed and new
layer formed.

Aphids, leeches, fleas, lice, Nutrient-rich fluid from the living host; is sucked by
mosquitoes, housefly, modified mouth parts;
Fluids or Fluid feeding;
vampire bats/
soft tissues
Tapeworm, Trypanosoma;
Already digested food is absorbed across the integument;
Substrate feeding Insect larvae / earthworms; Non-selective swallowing of mud, silt, sand, etc after
/ deposit feeding; burrowing their way through the food / organic material;

Land snail, caterpillar, May involve scraping and boring (termites, snails) /
Large
termites, snakes, birds, Capturing and swallowing (snakes, birds, dogfish, seals) /
particles
Bulk feeding / seals, squids, many Capturing, chewing and swallowing (squid, mammals) /
macrophagous mammals, spiders, blowfly Capturing, digesting externally and ingesting (spider,
feeding; larvae, crabs, dragonfly, etc. starfish, blowfly); using appendages like tentacles/pincers,

claws/ poisonous fangs and jaws/ mandibles;

THE HUMAN DIGESTIVE SYSTEM
The human digestive system consists of:

1. Alimentary canal: Mouth, throat, oesophagus, stomach, small intestine (duodenum, jejunum and ileum), large
intestine (colon, caecum and appendix), rectum and anus.

2. Accessory structures: Teeth, tongue, salivary glands, liver, gall balder and pancreas. These are organs, glands, and
tissues that enable digestive processes, e.g. by secreting fluids /chemicals, but the food does not actually pass through them.
COMPARISON OF HISTOLOGY OF GASTROINTESTINAL TRACT REGIONS
WALL LAYER STOMACH DUODENUM ILEUM COLON

Areolar connective tissue, same composition as mesenteries

Serosa (Adventitia) It is called serosa when the outermost layer lies adjacent to the peritoneal cavity.
It is called adventitia when the outermost layer is attached to surrounding tissue.
Muscularis externa Consists of three muscle layers: (i) inner oblique layer (ii) middle circular layer (iii) outer longitudinal layer

Network of unmyelinated nerve fibers and ganglia between Muscularis externa longitudinal and circular muscles
Brings about peristalsis when stimulated by pressure of food in the gut.

Auerbach’s plexus Receives impulses from the vagus nerve

(Myenteric plexus) Control of nerve impulses is involuntary

Promotes secretion of intestinal juices
Causes sphincter muscles to open, thus permitting food to pass from one part of the digestive system to another
Consists of loose connective tissue, collagen, large arteries and veins, lymph vessels and nerves
 Brunner’s glands Brunner’s glands present Brunner’s glands Brunner’s glands
absent. Brunner’s glands secrete absent. absent.
alkaline mucus to neutralize
No goblet cells Goblet cells
Submucosa acidic chyme from the stomach
present
Brunner’s glands are
compound, tubular, mucous

Goblet cells present

Meissner’s plexus Nerve network of unmyelinated nerve fibres and associated ganglia located with the submucosa
(Submucosal plexus) It is believed to work against the myenteric plexus to control the muscular contractions more finely.
In intestines, it works with Auerbach’s plexus in producing peristaltic waves and increasing digestive secretions.
WALL LAYER STOMACH DUODENUM ILEUM COLON
Mucosa 1. Muscularis mucosa:
Thin layer of smooth muscle at the boundary between mucosa and submucosa.

Contains both circular and longitudinal muscles

Functionally, the Muscularis mucosa presumably causes stirring at mucosal surface for increased secretion and
nutrient absorption
2. Lamina propria:

Formed by a very cell-rich loose connective tissue (fibroblasts, lymphocytes, plasma cells, macrophages,
eosinophilic leucocytes and mast cells).

Lamina propria contains numerous cells with immune function to provide an effective secondary line of defense
e.g. Peyer’s patches which are lymphoid structures located in the ileum.
Lamina propria of villi includes lacteals (lymphatic capillaries).
Lamina propria of intestinal villi may include smooth muscle fibers.
In oral cavity and oesophagus, lamina propria is located immediately beneath a stratified squamous epithelium

3. Surface epithelium:
Mucosal epithelium is highly differentiated along the several regions of the GI tract.

At the upper and lower ends of the tract, the epithelium is protective, stratified squamous.

Along the lining of the stomach, small intestine, and colon, the epithelium is simple columnar

In the stomach, surface epithelium contains mucous cells that secrete protective, alkaline mucus

(a) Plicae of the small intestine are permanent folds in the mucosa supported by a core of submucosa.
Plicae increase the absorptive surface area of the mucosa.

(b) Gastric pits are shallow indentations in surface epithelium of stomach mucosa into which gastric glands open.

(c) Intestinal crypts (crypts of Lieberkühn) contain secretory Paneth cells at the deep end, which
secrete lysosomal enzymes that contribute to protecting cells in the crypt lining.

(d) Villi are very small, typically densely-packed, invaginations of a mucosa that increase the surface
area for absorption. In the stomach – no villi, duodenum – many, leaf-like villi, ileum – few, finger-like
villi.
(e) Rugae are distensible folds in the gastric mucosa.

SECRETIONS FROM CELLS LOCATED IN THE GASTRIC WALL

The secretions of the mucous cells, chief cells, and parietal cells are known collectively as gastric juice, whose components
include: mucus, pepsinogen, hydrochloric acid and intrinsic factor

Type of Cell Secretion Stimulus for secretion Function

Mucous Cells Mucus Tonic secretion, with Physical barrier between lumen and stomach lining.
(i) Mucous surface cells irritation of mucosa

(ii) Mucous neck cells Bicarbonate Secreted with mucus Buffers gastric acid to prevent damage to epithelium

Pepsinogen Pepsin digests protein, including collagen

Gastric lipase Digests lipids
Acetylcholine, acid
Chief / Peptic / zymogenic cells
Prochymosin secretion. Rennin curdles soluble Caseinogen (milk protein) into
 (Prorennin) insoluble casein whose slow flow enables digestion

Hydrochloric acid (i) Activates pepsinogen to pepsin, Prorennin to rennin

(ii) Kills bacteria. Only Helicobacter pylori, that cause
gastritis and gastric ulcers survive in the stomach

Complexes with vitamin B12 to enable absorption of

Parietal / oxyntic cells Acetylcholine, gastrin, Vitamin B12 necessary for red blood cell formation
histamine
Vitamin B12 is a cofactor of enzymes which
Intrinsic factor synthesise tetrahydrofolic acid, which, in turn, is
needed for the synthesis of DNA components

Little intrinsic factor causes pernicious anemia

Enteroendocrine cells (APUD-cells: amine precursor uptake and decarboxylation cells)

(a) G cells Acetylcholine, peptides, (i) Stimulates secretion of gastric juice

and amino acids
(Gastrin-producing cells) Gastrin hormone (ii) Increases contractions of gastro-intestinal tract
(iii) Relaxes the pyloric sphincter.

(i) Inhibits stomach secretion of gastrin and HCl

(b) D cells Somatostatin (ii) Inhibits duodenal secretion of secretin and

Acid in stomach
(Somatostatin-producing cells ) hormone cholecystokinin
(iii) Inhibits pancreas secretion of glucagon
(i) Induces smooth muscle relaxation

(c)VIP-producing cells (vasoactive Vasoactive intestinal Distension of the (ii) Inhibits gastric acid secretion
intestinal peptide) peptide stomach wall (iii) Stimulates pepsinogen secretion by chief cells

(d) Enterochromaffin cells Histamine Acetylcholine, gastrin Stimulates gastric acid secretion
(Serotonin-containing cells)
DIGESTION

Digestion is the process by which large food molecules are broken down into small soluble molecules which can be absorbed
and assimilated into the tissues of the body.

Digestion includes two types of processes:

Mechanical processes: which include the chewing and grinding of food by the teeth and also the churning and mixing of
the contents of the stomach to expose more surface area to the enzymes that finish the digestive process.

Chemical processes: which include hydrolysis action of digestive enzymes, bile, acids.

DIGESTION IN THE MOUTH

It starts with chewing (mastication), which breaks food into pieces small enough to be swallowed and also increases the
surface area of food to digestive enzymes.

The sight, taste, smell and thought of food induces salivary glands to secrete saliva, a watery fluid with PH of 6.8 to 7.0.
During chewing, saliva mixes with food and the different saliva components perform different functions:

(i) Salivary amylase (ptyalin) enzyme catalyses the breakdown of amylose of cooked starch into maltose.
(ii) Water moistens food and binding it together for swallowing

(iii) Mucin binds and lubricates food; to enable swallowing.

(iv) Chloride ions activate salivary amylase

(v) Lysozymes kill bacteria in the buccal cavity.

NOTE:
Amount of amylase secreted in saliva depends on amount of starch the animal regularly feeds on in diet.

1. Amylase is usually absent in the saliva of carnivores because of absence of cooked starch in the diet.

2. In separate human groups, the relative amounts of amylase (in arbitrary units) produced in saliva were as follows:

Tswana: 248, Bushmen 22, European: 101. Which human group’s diet is largely made of flesh?
TYPICAL EXAMINATION QUESTION
(a) Describe the process of swallowing food in humans. (10 marks)
(b) Explain the role of gastric juice during food digestion in adult humans (10 marks)
DIGESTION IN THE STOMACH

Arrival of food in the stomach stimulates secretion of gastrin hormone from G-cells into the blood stream, which
stimulates the gastric glands to secrete gastric juice, whose components include: mucus, pepsinogen, hydrochloric acid
and intrinsic factor.

The components of gastric juice are secreted by different cells and perform different roles as follows:

Type of Cell Secretion Function

Mucous cells Mucus Forms a barrier at the stomach lining, to prevent tissue digestion.

(i) Mucous surface cells Bicarbonate Buffers gastric acid to prevent damage to epithelium
(ii) Mucous neck cells
Pepsinogen Pepsinogen on activation to pepsin digests protein to polypeptides
Gastric lipase Digests lipids to fatty acids and glycerol
Chief / Peptic / zymogenic
Prochymosin Rennin coagulates soluble milk protein Caseinogen into insoluble
cells
(Prorennin) casein in babies, whose slowed flow enables digestion by pepsin.
Gastric lipase Gastric lipase weakly hydrolyses fats to fatty acids and glycerol

(i) Activates pepsinogen to pepsin, Prorennin to rennin

(ii) Kills most bacteria in the stomach.

Hydrochloric acid
(iii) Provides optimum acidic pH for pepsin to hydrolyse
proteins into polypeptides.
Parietal / oxyntic cells (v) Stops the working of salivary amylase enzyme

Forms a complex which enables absorption of vitamin B12 that is

necessary in red blood cell formation
Intrinsic factor
Little intrinsic factor causes pernicious anemia

MECHANISM OF HYDROCHLORIC ACID SECRETION IN PARIETAL CELLS

 Due to churning by the stomach wall (alternate contractions and relaxations), VIP-producing cells are stimulated to
secrete the hormone called vasoactive intestinal peptide, which causes relaxation of pyloric sphincter muscle to allow the
semi solid chyme flow from the stomach into the duodenum, after a maximum of about four hours.
DIGESTION IN THE DUODENUM

Arrival of partially digested, acid food mixture in the duodenum stimulates endocrine cells in duodenal walls to secrete the
hormones: Secretin, Enterogastrone, Cholecystokinin (CCK) formerly Cholecystokinin-Pancreozymin (CCK-PZ),
Villikinin and Enterocrinin. These hormones coordinate activities of the stomach, pancreas, gall bladder and ileum as
follows:
Hormone Stimulus for secretion Effect

Stimulates the liver to secrete bile into the gall bladder.

Stimulates pancreatic secretion of non-enzymatic substances (hydrogen
Acid chyme in carbonate ions) from acinar cells. HCO - neutralise the acid from the
Secretin hormone duodenum 3

stomach to provide an alkaline pH optimum for pancreatic enzymes.

Inhibits secretion of HCl by oxyntic cells as chyme leaves the stomach.

Reduces stomach motility

Inhibits oxyntic cells from secreting hydrochloric acid in order to provide

an optimum pH for pancreatic enzymes.
Enterogastrone Acid and fat in the
Signals the stomach to empty slowly when fat is present, allowing much
hormone duodenum
time for digestion of fat already emptied.

NOTE: High fat diets stimulate enterogastrone production, which prolongs

food stay in the stomach, and is therefore useful in treating duodenal ulcer.

Stimulates contraction of gall bladder to release bile into duodenum.

(i) Bile salts (sodium glycocholate) emulsify fats i.e. fats physically break into
droplets due to reduced surface tension, which increases their surface area

Stimulates the pancreas to secrete pancreatic enzymes:

Cholecystokinin
(i) Pancreatic amylase which catalyses the hydrolysis of starch into
hormone maltose
Partially digested fat
(CCK) and protein in the (ii) Enterokinase, a non-digestive enzyme which activates Trypsinogen to
formerly called duodenum
Trypsin.
Cholecystokinin
(iii) Trypsinogen, which is activated by enterokinase to
Trypsin. Trypsin:
(1) Catalyses hydrolysis of polypeptides to peptides.
(2) Activates chymotrypsinogen to chymotrypsin.

(iii) Chymotrypsinogen, which is activated to chymotrypsin by Trypsin.

Chymotrypsin catalyses hydrolysis of casein / polypeptides into peptides.

Villikinin Alkaline pH in the Increases peristalsis in the small intestine and ileum villi movements, in
(Motilin) duodenum preparation for incoming food.

NOTE:
1. Some sources indicate that enterogastrone refers to any of the hormones secreted by the mucosa of the
duodenum in the lower gastrointestinal tract in response to dietary lipids to inhibit churning e.g. (i) Secretin (ii)
Cholecystokinin
2. All proteolytic (protein digesting) enzymes along the gut are secreted in inactive (precursor) form to prevent autolysis

(self-digestion) of gut tissues, which are protein in nature.

The churning action of duodenal walls turns the semi-solid Chyme into a thin, milky-looking alkaline fluid called Chyle.

DIGESTION IN THE ILEUM

Distention of the small intestine by food / tactile stimulus /
irritating stimulus stimulates the secretion of intestinal juice
(Succus entericus), which consists of a mixture of substances from
crypts of Lieberkühn and Brunner’s glands. Some of the
components of Succus entericus include the following enzymes:

Peptidases: catalyse hydrolysis of peptides into amino acids,

thereby completing the digestion of proteins.

Nucleotidases: catalyse hydrolysis of nucleotides into

phosphoric acid, nitrogenous bases and pentose sugars.

Maltase: catalyses hydrolysis of maltose into glucose molecules,

thereby completing starch digestion.

Sucrase (invertase): catalyses hydrolysis of sucrose into glucose

and fructose molecules.

Lactase: catalyses hydrolysis of lactose into glucose and
galactose molecules.
Intestinal lipase: catalyses hydrolysis of lipids into fatty acids
and glycerol.
Intestinal amylase: catalyses hydrolysis of starch into maltose.
FOOD ABSORPTION
It is the process by which soluble food substances are absorbed across the gut epithelium into blood circulatory system or

lymphatic system to be carried to all body cells.

During absorption, substances move as follows:

(i) From intestinal lumen across the free end / apical end / mucosal end of the absorbing cell.
(ii) Across the base / basilar end / serosal end of absorbing cell into the subcellular space, and finally into
blood circulatory system or lymphatic system.

NOTE: Substances entering at the apical surface may be metabolized or within the cell or may appear at the basilar surface
when changed into another form.

MAIN SITES OF NUTRIENT ABSORPTION

PROCESSES INVOLVED IN ABSORBING DIGESTED FOOD
(1) Simple diffusion (2) Facilitated diffusion (3) Active transport: Direct active transport and Secondary active transport

SECONDARY ACTIVE TRANSPORT

A form of active transport across a biological membrane in which a transporter protein couples the movement of an ion (e.g.
Na+ or H+) down its electrochemical gradient to the uphill movement of another molecule or ion against a
concentration/electrochemical gradient. Thus, energy stored in the electrochemical gradient of an ion is used to drive the
transport of another solute against a concentration or electrochemical gradient.

TYPES OF SECONDARY ACTIVE TRANSPORT

1. Cotransport (also known as Symport) 2. Exchange (also known as Antiport)
1. COTRANSPORT: The direction of transport is the same for
both the driving ion and driven ion/molecule.

Examples:

(i) The Na+/glucose cotransporter in enterocytes (small

intestine epithelial cell) and kidney proximal tubule epithelial
cells simultaneously transports 2 Na+ ions and 1 glucose
molecule into the cell across the plasma membrane.

(ii) The H+/dipeptide or tripeptide cotransporter in

epithelial cells of small intestine couples the downhill movement
of H+ across the plasma membrane to the uphill transport of
dipeptides and tripeptides into the cell against a concentration
gradient.

2. EXCHANGE: The driving ion and driven ion/molecule move

in opposite directions.

Example:
The Na+/Ca2+ exchanger in cardiac muscle cells transports 3 Na+
ions into the cell in exchange for 1 Ca2+ ion transported out of the
cell.

MECHANISMS OF ABSORBING DIGESTED FOOD IN THE ILEUM

Digested food Mechanism Description of the mechanism

Secondary active Glucose and galactose are cotransported into epithelial cells of
transport with Na+ villi with Na+ ions, then exported into blood capillaries by
Glucose and galactose
(Cotransport with Na+) facilitated diffusion.

Fructose moves into epithelial cells of villi by facilitated

Fructose Facilitated diffusion diffusion, then exported into blood capillaries by facilitated
diffusion.

Secondary active Amino acids are cotransported from intestinal lumen into small
transport with Na+ intestinal epithelial cells with Na+ ions, then exported to
Amino acids
(Cotransport with Na+) capillaries by facilitated diffusion.
 Oligopeptides (dipeptides and tripeptides) are cotransported
from intestinal lumen into villi epithelial cells with protons (H+)
Secondary active
Dipeptides and Tripeptides Oligopeptides are then hydrolysed by cytoplasmic peptidases
transport with H+
(Oligopeptides) into amino acids, which are exported from the villi epithelial
(Cotransport with H+)
cells into blood capillaries by facilitated diffusion.
Short chain fatty acids move into epithelial cells of villi by

Short chain fatty acids Simple diffusion simple diffusion, then are exported into blood capillaries by
simple diffusion.

Monoglycerides and long chain fatty acids diffuse into columnar

epithelia of villi, recombine to form lipids, then combine with
Monoglycerides and Long
Simple diffusion proteins to form water soluble lipoproteins called
chain fatty acids
chylomicrons, which are exported by exocytosis to lacteals.

NOTE:
1. Absorption of whole proteins occurs only in a few circumstances e.g. newborns when suckling absorb antibodies
(immunoglobulins) from the mother’s milk (colostral milk) to acquire passive immunity.

2. In adults, absorption of whole protein can cause allergic reaction due to presence of foreign protein in blood.
 ILEUM – THE MAJOR SITE FOR ABSORPTION
Adaptations of the ileum to absorption of food
(i) Ileum is long and highly folded for increased surface area in absorption of soluble food substances.
(ii) Ileum has numerous finger-like projections called villi which increase the surface area for absorption of soluble food.

(iii) Ileum epithelial cells have microvilli which further increase the surface area for efficient food absorption.

(iv) Ileum epithelium is thin to reduce diffusion distance for soluble food substances to allow fast rate of diffusion.
(v) Ileum epithelium is permeable to allow movement of soluble food substances across with minimum resistance.
(vi) Ileum villi have dense network of blood capillaries to rapidly carry away digested food from the absorption area
which maintains a steep diffusion gradient.

(vii) Ileum villi have permeable lacteal, a branch of the lymphatic system for carrying away fats

(viii) Ileum epithelial cells have numerous mitochondria to generate ATP energy for active transport of some ions.
(ix) Ileum inner surface is lined with a lot of mucus to prevent autolysis (self-digestion) by proteolytic enzymes.
TYPICAL EXAMINATION QUESTIONS
1. (a) Explain how the structure of villi in the small intestine is related to absorption of digested food.
Large surface area by microvilli / protrusion of exposed parts for fast uptake of soluble substances.

Epithelium only one layer thick to reduce diffusion distance.

Protein channels allow facilitated diffusion and active transport.

Numerous mitochondria provide much ATP for active uptake of some nutrients like glucose and salts.

Blood capillaries close to epithelium/ surface to reduce diffusion distance during absorption of glucose/ amino acids

Lacteal / lymphatic vessel is permeable/has large surface area at centre to absorb fatty acids and glycerol.

Tight junctions between adjacent villi enable controlling absorption of substances

 Rate of absorption

By living By poisoned
intestine intestine
Glucose 1.00 0.33
Galactose 1.10 0.53
Fructose 0.43 0.37
Xylose 0.31 0.31
Arabinose 0.29 0.29
(b) The table below shows experimental results of the rate of absorption of hexose sugars (Glucose, galactose and fructose),
and pentose sugars (xylose and arabinose) by pieces of living intestine and by pieces of intestine poisoned with cyanide. The
results are shown as relative to the rate for glucose.

(i) Explain the observed rates of sugar absorption shown by the two tissues.

The rate of absorption of glucose and galactose is faster in living intestine; but much
slower in poisoned intestine; because absorption of these sugars is active transport
requiring ATP whose formation depends on enzymes; which are inhibited by respiratory
inhibitor cyanide; To a small extent, the two sugars are absorbed passively;

Rate of absorption of fructose, xylose and arabinose is the same or relatively the same
in living intestine and in poisoned intestine; because absorption of these sugars is
facilitated diffusion which does not require ATP; therefore not inhibited by respiratory
poison cyanide;

2. The graph below shows how an injection of secretin affects the secretion of pancreatic juice by the pancreas.
PROBABLE SOLUTIONS
(a) Secretin injection causes a rapid increase in the volume of pancreatic juice from 20 minutes to 30 minutes; followed by gradual decrease to 40
minutes; then a rapid decrease to 60 minutes;

Secretin injection causes gradual increase in the concentration of bicarbonate ions from 20 minutes to 30 minutes; followed by rapid increase to a peak at
40 minutes; then rapid decrease until 60 minutes;

Secretin injection causes gradual decrease in concentration of amylase from 20 minutes to 30 minutes; followed by rapid decrease to a minimum at 40
minutes; then gradual increase until 55 minutes and thereafter remains constant until 60 minutes;

Upon injection into blood, secretin hormone circulates to reach the pancreas and liver, first in low concentration from 20 minutes to 30 minutes; gradually
stimulating pancreatic secretion of watery hydrogen carbonate ions from acinar cells and gradually stimulating secretion of somatostatin hormone
which gradually inhibits secretion of pancreatic amylase enzyme.

From 30 minutes to 40 minutes, there is now much secretin concentration in blood circulation; which rapidly stimulates pancreatic acinar cells to rapidly
secrete hydrogen carbonate ions and also greatly stimulates secretion of somatostatin hormone which rapidly inhibits secretion of pancreatic amylase
enzyme;

From 40 minutes to 60 minutes, high PH (alkalinity) due to hydrogen carbonate ions inhibits the working of secretin hormone; causing less stimulation
of acinar cells hence rapid decrease in secretion of hydrogen carbonate ions. Somatostatin hormone secretion decreases hence decreasing the inhibition of
pancreatic exocrine cells causing increased amylase enzyme secretion;

(b) (i) Pancreatic juice is mainly composed of substances (like water), hydrogen carbonate ions, and small amounts of enzymes like amylase.

(ii) Secretion of bile in liver cells, stored in the gall bladder which when released in the duodenum emulsifies fats into droplets, which is physical digestion.

(c) (i) Conditioned reflexes from vagal centre in the brain fail to stimulate secretion of acetylcholine, no secretion of gastrin hormone, no secretion
of gastric juice (HCl) during the cephalic phase (before food reaches the stomach) hence the stomach wall will be less irritated.

(ii) Blocking the action of acetylcholine using atrophine inhibits the secretion of gastrin hormone; hence secretion of gastric juice (HCl) is inhibited.
COLON
In the colon, there is mainly absorption of:
(i) Water into the blood capillaries by osmosis.
(ii) Vitamins Biotin (B7) and K, which is synthesised by Escherichia coli bacteria that live in the colon.

(iii) Na+, Cl- and K+

NOTE: The colon wall contains mucus secreting cells for lubricating the movement of undigested food through the colon.

APPENDIX AND CAECUM

In ruminants like cattle and in non-ruminants like rabbits, mutualistic bacteria secrete cellulase enzyme which digests
cellulose to glucose, which is lost along with faeces. In the process described as coprophagy (coprophagia), rabbits eat own
faecal pellets while dung beetles feed on cow dung to enable absorption of glucose at the ileum.

In humans, appendix and caecum have no obvious role.

RECTUM
In the rectum, food is stored temporarily to enable osmotic absorption of water into blood capillaries.

CONTROL OF DIGESTION IN HUMANS

A combination of hormonal and nervous stimulations and inhibitions of the gut that regulate the secretion of digestive
juices in the gut.

IMPORTANCE OF CONTROL OF DIGESTION

(i) Secretion of digestive juices depends on respiratory energy, therefore unnecessary secretion must be prevented to
avoid wastage of respiratory substrates.

(ii) Secretion of proteolytic enzymes in inactive form prevents autolysis (self-digestion of tissues).

MECHANISMS OF CONTROLLING DIGESTION IN HUMANS

Involves a combination of hormonal and nervous; stimulations and inhibitions of the gut; that regulate the secretion of
digestive juices in the gut;

The digestive juices secreted include saliva in the buccal cavity; gastric juice in the stomach; pancreatic juice and bile in
the duodenum; intestinal juice in the ileum;

CONTROL IN THE MOUTH

Sight / smell / thought of food stimulate conditioned reflexes involving the cerebral cortex, hypothalamus and medulla
oblongata; which stimulate salivary glands to secrete saliva.

Contact of food with tongue taste receptors stimulates nerve impulses via sensory neurons to the hypothalamus and
medulla oblongata; relayed along motor neurons to stimulate salivary glands to secrete saliva.

-Salivary amylase in saliva causes hydrolysis of starch to maltose.

Loss of appetite / depression inhibit cerebral cortex; parasympathetic centre is not stimulated, no secretion of saliva;

CONTROL IN THE STOMACH

Occurs in 3 phases: cephalic; gastric; and intestinal phases;

Cephalic phase / Nervous phase:

It occurs before food enters the stomach;

Sight / smell / thought of food stimulate conditioned and unconditioned reflexes; involving the cerebral cortex,
hypothalamus and medulla oblongata; which stimulate the vagus nerve causing the release of acetylcholine; which
stimulates the secretion of the hormone gastrin; whose effects are:

(i) Stimulates secretion of gastric juice.

(ii) Increases contractions of gastro-intestinal tract

(iii) Relaxes the pyloric sphincter to let in bolus of food from the gullet;

Loss of appetite / depression inhibit cerebral cortex; parasympathetic centre is not stimulated, no gastric secretion;

NOTE:

Secretion of nervous phase lasts for about one hour during which gastric juice secretion reaches a maximum, after
which there is a rapid decrease from 1 hour to 1.5 hours.

Therefore, nervous secretion is: (i) short lasting and (ii) rapid as compared to the hormonal phase.
Gastric phase:
Arrival of food bolus distends / stretches the stomach wall which activates stretch receptors to fire impulses to the

Meissner’s plexus in the stomach wall to cause the following effects:

(i) Stimulate local secretory reflexes in the stomach wall to activate gastric glands secrete pepsinogen and HCl;

(ii) Stimulate reflexes in the medulla, via the vagus nerve to activate gastric glands wall to secrete pepsinogen and HCl;

(iii) Stimulate enteroendocrine cells / G-cells to secrete gastrin hormone; which stimulates secretion of gastric juice;
(iv) Stimulate enteroendocrine /enterochromaffin cells to secrete histamine; which activates secretion of gastric juice;

Partially digested proteins especially peptides / decrease in pH activates chemoreceptors, which stimulate G-cells to
secrete gastrin hormone; which stimulates secretion of gastric juice;

Excessive acidity (PH of less than 2) inhibits G-cells hence gastric juice secretion reduces;

Emotional upset activates sympathetic nervous system whose effects override the parasympathetic nervous system;

NOTE:
The gastric glands are stimulated by hormones to secrete gastric juice for about four hours.
Therefore, hormonal secretion is: (i) longer lasting and (ii) gradual as compared to the cephalic phase.

Intestinal phase:
Distension of duodenum / presence of acid chyme / partially digested food stimulates the secretion of intestinal (enteric)
gastrin hormone; which stimulates secretion of gastric juice in the stomach;

Distension of duodenum / presence of acid chyme / fatty acids / irritants / in the duodenum stimulates the secretion of
Intestinal hormones:

(i) Secretin; which stimulates the release of bile from the liver and hydrogen bicarbonate ions in pancreatic juice;

(ii) Cholecystokinin; which stimulates the pancreas to secrete its enzymes;

(iii) Enterogastrone; which inhibits/suppresses gastric activity (any further secretion of acid by the stomach);
(iv) Vasoactive intestinal peptide inhibits gastric acid secretion.

Distension of duodenum / presence of acid chyme / fatty acids / irritants / in the duodenum initiates gastric-inhibitory
impulses in the enterogastric reflex causing suppression of gastric activity; and emptying of stomach;

CONTROL IN THE ILEUM

Contact of food with intestinal lining stimulates the intestinal glands; to secrete intestinal juice composed of enzymes
responsible for completion of digestion of food substrates;

Variations in volume of gastric juice produced by nervous, hormonal and mechanical stimulations with time after eating food
OBSERVATIONS / DESCRIPTION

1. Volume of gastric juice produced during nervous stimulation increases rapidly from 0 hour to a maximum at 1 hour, then
decreases rapidly and ceases at 1.5 hours. Nervous secretion is: (i) shorter lasting (ii) instantly rapid as compared to hormonal and
mechanical phases.

2. Volume of gastric juice produced during hormonal stimulation increases gradually from 0 hour to 1 hour, then increases rapidly
to a maximum at about 2.5 hours, then decreases rapidly and ceases at about 3.3 hours.

Therefore, hormonal secretion is: (i) longer lasting and (ii) initially gradual as compared to the cephalic phase.

3. Volume of gastric juice produced during mechanical stimulation (food stretching stomach and duodenal wall) increases
gradually from 0 hour to 0.7 hour, then increases rapidly to a maximum at about 1.6 hours, then decreases rapidly and ceases at about
2.6 hours
TYPICAL EXAMINATION QUESTION

The graph below shows the amount of gastric juice produced by the stomach of an individual who had just chewed some
food. The food was spat out after being chewed, and none was swallowed.

(a) Name two constituents of gastric juice

(b) Assuming that no traces of food got

down into the stomach, explain how the secretion
of gastric juice was brought about.

(c) (i) How much time elapsed between the

moment the food was spat out and the moment
gastric juice started to be produced?

(ii) Account for the delay in (c) (i) above.

(d) If the stomach of an adult person is
surgically removed through an operation, suggest
with reasons, the more suitable diet for such a
person after recovery from the operation.

ASSIMLIATION OF FOOD
Assimilation: The process by which simple soluble food substances are absorbed and used by body cells in the various ways.
The products of digestion are brought directly through the hepatic portal vein to liver, which controls the amount of nutrients
released into the mainstream blood circulatory system.

Assimilation supports growth, development, body renewal, and storing up of reserves used as a source of energy.
Metabolism: Chemical processes within cells of an organism.
It involves:

(i) Catabolism: Break down of complex molecules into simpler molecules, with release of energy.

(ii) Anabolism: Assembly / building up of complex molecules from simple molecules using energy.

FOOD HOW ABSORBED FOOD IS USED IN THE BODY HOW BODY DEALS WITH EXCESS
 ATP synthesis in respiration Stored in the liver as glycogen.
Formation of glycoproteins involved in cell to cell
recognition mechanisms.
Excess carbohydrates may be converted
Glucose
For production of mucus into fats for storage.
Excess carbohydrates are stored in the form of glycogen in
the liver and muscles.

Formation of protoplasm of cells during growth

Production of enzymes and antibodies

Formation of body structures such as hairs, nails, hooves,

Deaminated in the liver to form urea,
cell membranes
which is expelled by kidneys.
Amino acids
Oxidised to release ATP energy during severe starvation i.e.
Some amino acids are transaminated
in the absence of glucose and fats.
to produce a different amino acid
Formation of hormones e.g. insulin

Formation of plasma membrane components e.g.

glycoproteins, channel proteins

The long chain fatty acids are desaturated in the liver and
are then broken down to carbon dioxide and water by
successive oxidations.
Fatty acids
Some of it can be converted into glucose Stored as fat under the skin
and glycerol
Some used to form various structures which are components
of cells e.g. phospholipids
TYPICAL EAMINATION QUESTION
(a) What roles do the liver and pancreas play in: (i) food digestion (ii) metabolism of absorbed products
(b) How can the diet of raw liver prevent the disease pernicious anaemia?
Digestion Metabolism of absorbed products

Pancreas On stimulation by cholecystokinin hormone, the (i) If in excess (above 90mg/100cm3), the
pancreas secretes enzymes whose effects are as pancreas is stimulated to secrete insulin hormone
follows: which causes conversion of glucose to glycogen for
storage, fat or metabolizing it to energy and CO2.
(i) Amylase catalyses hydrolysis of starch into
maltose (ii) If little (below 90mg/100cm3), the pancreas is
(ii) Enterokinase enzyme which activates stimulated to secrete glucagon hormone which causes
Trypsinogen to Trypsin. conversion of glucagon to glucose hence increasing the
blood glucose level.
(iii) Trypsin:

(1) Catalyses hydrolysis of polypeptides to peptides.

(2) Activates chymotrypsinogen to chymotrypsin.

(iii) Chymotrypsin catalyses hydrolysis of

casein / polypeptides into peptides.

(iv) Lipase hydrolyses fats to fatty acids and glycerol

(v) Nuclease hydrolyses nucleic acids to nucleotides

(vi) Polypeptidase hydrolyses polypeptides to

amino acids.

On stimulation by secretin hormone, the pancreas

secretes hydrogen carbonate ions from acinar cells,
which neutralise the acid chyme from the stomach to
provide an alkaline pH optimum for pancreatic

enzymes.
Liver On stimulation by secretin hormone, the liver secretes 1. The Liver regulates blood glucose:

bile into the gall bladder. (i) If in excess (above 90mg/100cm3),

glucose is converted into glycogen for storage.

(ii) If little (below 90mg/100cm3),

On stimulation by CCK hormone, gall bladder
glycogen is converted into glucose for use.
contracts to release bile salts which emulsify fats i.e.
fats physically break into droplets due to reduced 2. The liver regulates amino acids in the
surface tension, which increases their surface area body: Excess amino acids are not stored in the body,
but undergo deamination process. i.e. the amino
group (- NH2) from the amino acid is removed to
form ammonia, which later forms urea that is carried
in blood to kidneys for excretion.
3. The liver regulates lipids (fats) in the
body: It synthesizes and degrades
phospholipids and cholesterol.
4. The liver forms red blood cells in foetus and
breaks down worn out red blood cells in adults.

5. The liver forms plasma proteins from amino acids

6. The liver stores fat soluble vitamins A, D, E,

K and water soluble vitamins B12 and C

7. The liver stores minerals like Iron,

potassium, copper, zinc and trace elements.
8. The liver detoxifies poisonous substances i.e. toxic

substances are turned harmless by the liver cells e.g.

alcohol, cholesterol and hydrogen peroxide.

(b) Raw liver is rich in vitamin B12 which is essential for formation of red blood cells (erythrocytes), whose absence
causes pernicious anaemia characterised by paleness, slowness and death.
FOOD AND DIET IN HUMANS
Food: Any substance taken in to nourish the body and sustain life. Food provides energy and nutrients.

Nutrient: is a substance which is needed for growth, repair and metabolism.

The three main nutrients are: (1) carbohydrates (2) proteins (3) lipids (fats and oils)

MEASURING FOOD ENERGY CONTENT

The energy content in a food sample can be measured by simple calorimetry.

Calorimetry: Measuring the amount of heat given out or taken in by a process, such as the combustion of a fuel.

PROCEDURE OF CALORIMETRY
(i) Pour cold water into a boiling tube / small beaker / metal
can
(ii) Record the starting temperature of the water

(iii) Measure accurately the mass of the food sample in a crucible Thermometer

(iv) Heat the food until it catches fire.

(v) Heat the water using the flame from the burning food Boiling tube or
small can
(vi) Record the final temperature of the water and
calculate the temperature difference. Water

NB: The experiment above can be done more accurately using a

food calorimeter, though it costs more money to purchase.

Calculations
Food sample
Work out the energy transferred to the water in joules or in calories in crucible
Energy transferred (J) =
Mass of water (g) × 4.2 (J/g°C) × temperature increase (°C)

Note: 4.2kJ (1 cal.) of energy are required to raise the

temperature of 1 kg of water through 10C

COMPARISON OF ENERGY VALUES

Worked example Carbohydrate: 1 gram contains 17 kJ

When 0.5 g of food is burned, 10 cm3 of water warms up by 20°C. Fat: 1 gram contains 39 kJ
What is the energy content of the food in J/g?
Protein: 1 gram contains 18 Kj

Solution
ENERGY UNITS
1 cm3 of water has a mass of 1 g Energy units are joules, no longer calories

Energy transferred to water = 10 × 4.2 × 20 = 840 J 4.18 joules = 1 calorie

Energy content of food = 840 ÷ 0.5 = 1680 J/g
1000 calories = 1 kilocalorie (kcal.) = 1 Cal
To find the energy value of sugar, 1g of sugar is burnt in a crucible,
1000 joule = 1 kJ (kilojoule) = 1 joule
the flame produced is used to heat 100 g water in a metal can and
1000 kJ = MJ (megajoule)
the rise in temperature of the water measured.

PRECAUTIONS
When comparing different foods, it is important to carry out a fair test by keeping other variables constant:
(1) Starting temperature of water (2) temperature increase (3) distance of the flame from the boiling tube

More reliable results can be obtained by repeating the experiment.

SOURCES OF ERROR IN CALORIMETRY

(a) Inaccurate weighing of sugar
(b) Incomplete combustion of the sugar

(c) Inability to measure the temperature difference accurately enough

(d) Heat from the burning sugar escaping without heating the water.
ENERGY-FOOD INTAKE AND CONSUMPTION
The body needs energy for three main reasons:

(i) Maintain the basal metabolic rate (BMR) – minimum energy a body requires at rest to perform vital
functions like beating of the heart, breathing, peristalsis, impulse transmission, synthesis of biological molecules like
proteins, etc.

(ii) Sustain body activities like muscle contraction during movement, locomotion, etc.

(iii) Generation of heat to maintain body temperature at about 370C

NOTE: BMR accounts for about 65% of the energy used in the body each day.

FACTORS WHICH DETERMINE BASAL METABOLIC RATE

Age, Sex, Body mass, Nature of physical activity engaged in, Muscle mass, Diet, Drugs, Environmental factors e.g.
temperature, Hormonal factors e.g. during pregnancy and lactation, Genetics.

(a) (i) Factors shown in the graph,

which affect BMR: Age and sex

(ii) Other factors not shown in the graph,

which affect BMR:

Muscle mass, Body size, level of physical

activity, and Pregnancy and lactation, Diet,
Drugs, Environmental factors e.g. temperature,
Hormonal factors e.g. during pregnancy and
lactation, Genetics

Explanation of variation in BMR with the factors in (a) (i) above.

Variation in BMR with sex

At about 2.5 years and below, BMR in males is equivalent to BMR in females because infants have basically identical composition of
carbohydrates, fats and protein.

From about 2.5 years throughout life, BMR is slightly higher in males than in females because males usually have more body muscle
than females while females usually have more fat than males per unit body mass and surface area. The more muscle tissue in the body, the
more energy the body needs just to function e.g. to conduct impulses and biosynthesis compared to fat cells that largely store fat, with little
biosynthesis.

Variation in BMR with age

Infants and children have relatively high BMR than old-aged adults because at infancy and childhood much of the energy consumed is
used in biosynthesis of cellular components required for growth. At adulthood, biosynthesis is greatly reduced since growth has stopped.

From the age BMR was first determined to about 20 years of age, BMR decreases rapidly, then remains constant up to about 50 years of
age and thereafter decreases slowly.

From infancy to maturity at 20 years of age, biosynthesis of cellular components required for growth decreases rapidly, then remains
constant by middle age until 50 years of age and thereafter decreases slowly, partly because of loss of muscle tissue, and also because of
hormonal and neurological changes. Only repair and replacement of worn out cells occurs at slow rate by adulthood.

Explanation of variation in BMR with the factors in (a) (ii) above.

Muscle mass (amount of muscle tissue in the body). Muscle requires more energy to function than fat. The more muscle tissue in the
body, the more energy the body needs just to exist.

Body size: Larger bodies tend to have a higher BMR because they usually have larger internal organs and fluid volume to maintain.
Taller people have a larger skin surface, therefore have higher metabolism to maintain a constant temperature.

Genetics: Genotypes and genetic disorders determine the rate of BMR.

Physical activity: Regular exercise increases muscle mass and causes the body to burn kilojoules at a faster rate, even when at rest.

Hormonal factors (e.g. during pregnancy and lactation): Hormonal imbalances caused by certain conditions, including hypo- and
hyperthyroidism, can affect the metabolism. Expectant and lactating mothers require more energy to support foetal and baby growth
respectively.

Environmental factors (e.g. temperature): Weather can also have an effect on body metabolism; if it is very cold or very hot, the body
works harder to maintain its normal temperature and that increases the metabolic rate.

Drug content in the body: Caffeine and nicotine can increase your metabolic rate, while medications including some antidepressants
and anabolic steroids can contribute to weight gain regardless of what you eat.

Diet: Certain aspects of one’s diet can also affect metabolism e.g. inadequate intake of iodine for optimal thyroid function can slow
down body metabolism.
BALANCED DIET

Balanced diet is one which contains the correct proportions and quantity of protein, carbohydrate, lipids, vitamins, mineral
salts, water and dietary fibre/roughage required to maintain health.

Mainly, carbohydrates and lipids are for energy production, proteins are for growth and repair, vitamins and mineral salts
are for protection of good health, water is a solvent while roughage stimulates peristalsis to prevent constipation.

An unbalanced diet can lead to deficiency diseases.

EFFECTS OF UNDERFEEDING AND OVERFEEDING

If energy output exceeds energy input, carbohydrate reserves (glycogen) and fat reserves (adipose tissue) are respired and
the person’s body mass decreases. When carbohydrate and fat reserves exhaust, tissue protein is respired and the body wastes
away.

If energy intake exceeds energy usage over a period of time, carbohydrate is turned into fat and the person’s body mass
increases leading to obesity (overweight).

Disadvantages of obesity: (1) the extra mass causes a person to get tired quickly (2) increases chances of stroke/heart attack.
How an obese person can lose weight: (1) Eating less energy food (2) Taking more exercises to increase energy output

BODY MASS INDEX (BMI)

This is one of the ways of determining whether a person is underweight or overweight.
BMI can be calculated using the formula:
BMI = Mass in kg

(Height in m)2

Qn. Calculate the BMI of a female of mass 69 kg and height of 1.67m

Another way of determining whether a person is underweight or overweight is to use a graph showing the relationship
between height and body mass.
CHANGES IN M ETABOLIC RAT
E AND ENER GY RESER VE
UTILISATION DURIN G STAR
VAT ION

CHANGES IN BODY ENERGY RESERVES DURING STARVATION

Starvation results from the inadequate intake of nutrients or the
inability to metabolize or absorb nutrients.

CAUSES OF STARVATION
Prolonged fasting, anorexia, deprivation, or disease
SYMPTOMS OF STARVATION

Weight loss, dehydration, apathy, listlessness, withdrawal, increased

susceptibility to infectious disease, discoloured hair color, flaky skin, and
massive edema in abdomen and lower limbs causing the abdomen to
appear bloated.

ADVERSE EFFECTS OF STARVATION

(i) Marasmus: occurs on account of extreme energy deficiency,

typically from inadequate amounts of protein and calories.

(ii) Kwashiorkor: is related to marasmus, affects children who

are protein-energy deficient, and can result in edema (fluidic
inflammation)

and an enlarged fatty liver — resulting in the counterintuitive distending of

bellies, giving the illusory impression that starving children are well fed.

INTERVENTIONS AGAINST STARVATION

Rehydration and feeding the starving person low-bulk food with much
proteins, much energy and fortified with vitamins and minerals. Avoid
foods high in bulk but low in protein content

DESCRIPTION OF CHANGES IN ENERGY RESERVES

Glycogen, proteins, and fats are all metabolized during starvation.

Exhaustion of blood glucose stimulates glucagon secretion and insulin

secretion is inhibited.

Within the first 24 hours, the very low glycogen amount stored in the
liver and muscles decreases rapidly to depletion because glycogen is
broken down into glucose for oxidation to release energy, while the
amounts of fats and protein remain high.

Anaerobic breakdown of glycogen in skeletal muscle is also stimulated.

Within week 1, a few hours after depletion of carbohydrate/glycogen, the amount of fats decreases rapidly while the amount
of protein decreases gradually until about 6 weeks of starvation.

This is because fats are hydrolysed rapidly into fatty acids and glycerol while oxidation of amino acids releases energy.

The liver metabolizes fatty acids into ketone bodies that are degraded to release energy. Accumulation of ketones causes

ketosis, by condition characterised by blood becoming acidic

Fatty acids in skeletal muscles are broken down to release energy, thus decreasing the use of glucose by tissues other than
the brain.

Glycerol is converted into small amount of glucose, but most of the glucose is formed from the amino acids of proteins.

The brain begins to use ketone bodies, as wells as glucose, for energy.

Dependency on fats for energy release decreases the demand for glucose, protein breakdown reduces but does not stop.

The liver degrades non-essential proteins into glucose for the brain in a process called gluconeogenesis, which involves
converting carbon skeletons into pyruvate or Krebs’ cycle intermediates and excreting amino groups from the body as urea.

From 6 weeks to 8 weeks, amount of fat decreases slowly to very low levels, while amount of protein decreases rapidly.

This is because as fat reserves / stores are getting depleted, metabolism of fats to release energy occurs gradually and the
body begins to rapidly break down essential proteins, leading to loss of liver and heart function as these organs are broken
down for fuel metabolizing proteins as the major energy source.

Muscles, the largest source of protein in the body, are rapidly depleted.

TYPICAL EXAMINATION QUESTIONS

A group of rats were encouraged to over eat by feeding them with unlimited supplies of processed foods such as chocolate and cakes over a
three week period. These rats were called cafetarian rats. Over the same period, another group of control rats fed on unlimited supplies of
their natural food. (i) What was the effect of
feeding the rats on food other
than their natural food? (1½
marks)

AVERAGE O
Cafetarian rats
Energy content of food eaten (kj) 11670
Gain in the body mass (g) 131
Gain in body fat (g) 66
Energy used (kj) 9440
They gained more body mass, fat and
energy

(ii) Determine the average

gain in mass of the cafetarian
rats over the control rats
during the 21 days Average gain
in mass = gain in body mass of
cafeterian – gain in body mass of
control rats = 131 – 103 = 28g

(iii) State three features of the two groups of rats which should be kept the same: Age, sex, species (1½ marks)

(iv) Which chemical of life in the rats would have been responsible for most of the gain in mass? Body fat (½ marks)

(c) Explain the observation that some people eat enormous amounts of foods without putting on weight where as others
become over-weight on quite small food intake: Weight gain does not only depend on food intake, but on other factors like genetic
makeup.
(d) Using evidence from the data, explain why cafetarian rats were able to gain more weight than control rats. (2 marks)
The difference between the energy content of food and energy used is higher in cafetarian rats; so unused food had to be converted to fat
(e) Why were control rats necessary in this experiment? For comparison of results (1 mark)

FEEDING EXPERIMENTS ILLUSTRATING THE IMPORTANCE OF VITAMINS IN NORMAL DIETARIES

In his investigations exploring the relationship between diet and

growth in rats, Frederick Gowland Hopkins found that a diet
consisting of protein, salts, fats, and carbohydrates could not alone
support growth.

EXPERIMENT
Two groups of young rats were used.
Group A were fed on a diet of purified casein, starch, glucose, lard,
minerals and water only for the first 18 days.

Group B were fed on a diet of purified casein, starch, glucose,

lard, minerals and water plus an extra of 3cm3 of milk daily for the
first 18 days.
After 18 days milk was given to group A rats and removed from
group B’s diet.

OBSERVATIONS
Group A rats increased in mass gradually from 0 day to 10 days,
mass decreased gradually until about 12 days, mass remained
relatively constant up to 22 days, then mass increased rapidly from
about 22 days to 50 days
Group B rats increased rapidly in mass from 0 day to 18 days, then gradually increased in mass from 18 days to about 23
days, stopped growing from about 23 days to 40 days and gradually decreased in mass/lost weight thereafter.

CONCLUSION: Hopkins’s experiments revealed that, to grow, animals needed small amounts of other substances he called

“accessory food factors”- now known as vitamins.

EXPLANATION
Group A rats resumed growth and increased in weight after 18 days while group B rats stopped growing and lost weight after 18
days. While the 3cm3 of milk had an insignificant food value in terms of carbohydrate, fat, protein and minerals, the milk contains
an extra nutrient which the rats needed to be able to grow and develop.

Why it was necessary to transfer milk from group B to group A half way through the experiment?
To ensure that all groups of rats are subjected to identical conditions e.g. feeding them on identical food so as to establish the effect
of milk on growth while eliminating the possibility of other factors being responsible the observed differences in results e.g. choice
of rats in one group (group A) may have been more sickly than those in group B etc.

Why feeding rats on one type of protein (casein), not a variety is ruled out as a possible cause of growth stoppage and weight
loss?

Although proteins are essential for growth and there are different types, proteins are hydrolysed in the body into different amino
acids, and the body is able to make some amino acids for itself. Therefore even though the rats were only getting casein this was
enough to not have an effect on growth.

Why while a diet of protein alone is sufficient for young animals, it is inadequate for adults?
Much as milk contains all the nutritional requirements like protein, carbohydrates (lactose), lipids, mineral salts, vitamins and
water, some amounts may be nutritionally insufficient to meet the metabolic demands of adults.

Some people who are lactose intolerant can’t digest the main sugar (lactose) in milk. In normal humans, production of lactase
enzyme that digests lactose stops between ages of two and five years, which would result in insufficient ATP production.

NUTRITION IN CARNIVORES AND HERBIVORES

(a) Carnivorous animals: are either predators or scavengers whose diet consists of mainly flesh obtained from preys.
(i) Predator: An animal that hunts and kills animals for food.

(ii) Prey: An animal that is hunted and killed for food.

(iii) Scavenger: An animal that eats dead animals, but doesn’t kill them.

(b) Herbivore: An animal whose diet is mainly vegetation

(i) Grazers: Mainly feed on grass

(ii) Browsers: Mainly feed on leaves of shrubs and trees

Carnivore Herbivore
Adaptations for Well-developed sense of smell for locating prey Upper jaw lacks incisors to provide a hard pad against
finding and which lower incisors press and cut grass.
Fast moving to outpace and capture prey
capturing prey
(carnivores) or Well-built body to manipulate and capture prey. Tongue is highly muscular for manipulating food
during chewing.
grazing /
Very sharp claws for gripping and killing prey.
browsing
(herbivores) Keen eye sight for locating prey from a distance
Foot pads enable stealth movement to ambush prey.
Long, sticky tongue for reaching distant prey e.g. toads.
Elongated canines for digging up prey e.g. walrus

Adaptations for Sharp pointed canines for tearing the fresh of prey Molars and premolars are ridged for maximum
ingesting the food grinding of hard cellulose materials.
Flat molars to crush prey
Incisors pointed for nipping and biting. Molars and premolars have large surface area for
maximum grinding of the hard cellulose materials.
Carnassial teeth present for shearing flesh.
Articulation of lower jaw permits lateral movement to
Upper jaw wider than lower jaw to facilitate shearing. enable maximum grinding of food.
Up-and-down jaw action only prevents lateral Well-developed jaw muscles provide much grinding
movement hence reducing the danger of dislocation power for crushing cellulose materials.
Powerful jaw muscles provide much force for chewing Between the front and cheek teeth, there’s a gap
called diastema for separating crushed grass from
uncrushed grass for effective chewing.

Adaptations for No cellulose in diet hence less developed caecum and Ruminant stomachs are four chambered to derive
digesting the food appendix to reduce on body weight to enable fast running. maximum nourishment from grass.

Relatively short alimentary canal reduces weight, since Mutualistic bacteria in caecum and appendix enable
diet is entirely protein. chemical digestion of cellulose into glucose.

Relatively long alimentary canal to digest vegetation

DIFFERENCES BETWEEN CARNIVORES AND HERBIVORES RELATED TO NUTRITION
Carnivores Herbivores

Closed pulp cavity in teeth Open pulp cavity in teeth

Upper jaw incisors present Upper jaw incisors absent in most herbivores

Canines present and well developed Canines small or absent to create a diastema

Carnassial teeth present Carnassial teeth absent

Cheek teeth pointed Cheek teeth flattened with enamel ridges and dentine grooves

Articulation of lower jaw prevents lateral movement Articulation of lower jaw permits lateral movement

Relatively short alimentary canal Relatively long alimentary canal

No cellulose digestion Cellulose digestion occurs in caecum

EXAMPLES OF SYMBIOTIC ASSOCIATIONS IN ANIMALS

Symbiosis: Ecological relationship between two or more organisms living together with some form of feeding relationship.

Mutualism: Close relationship where two organisms of different species depend on each other for reciprocal benefit, without
any harm e.g. pollination flowers by insects, Trichonympha and termites, cellulase producing bacteria and herbivores, etc.

Commensalism: Loose relationship in which two organisms of different species live together, only one organism benefits while
the other remains unharmed e.g. sea anemone and clown fish.

Parasitism: Close relationship between organisms of different species in which one organism called parasite obtains nutrients
from and harms a larger living organism called host.

DIGESTION IN RUMINANT MAMMALS

Ruminants: are the mammals, which have a 4-chambered stomach for the digestion of plant based food.
Rumination involves regurgitation of fermented grass known as cud, chewing and re-chewing it again to further break down
plant matter and stimulate digestion.

Ruminating mammals include cattle, goats, sheep, giraffes, deer, camels, antelope, etc.
Four-chambered stomach showing food movement during feeding
1. Rumen (Paunch): Bacteria and protozoa in the
rumen secrete cellulase enzyme which breaks down
cellulose into glucose which undergoes fermentation to form
organic acids, carbon dioxide and ethane. The
fermentation process produces heat that keeps ruminants
warm.

2. Reticulum (Honeycomb bag): Here any foreign

objects that may have been accidentally swallowed with
food settle out in the honeycomb structure of the
reticulum’s walls. Reticulum is sometimes called
“hardware stomach”.
 3. Omasum (Psalterium / Manyplies): Absorbs
water from food and also absorbs more nutrients called
volatile fatty acids that supply ruminants with energy.

4. Abomasum (Reed / True stomach): Here, the food particles are digested by hydrochloric acid in the same way it
occurs in human stomachs. The remaining particles are then passed on to the small intestine where most of the nutrients are
absorbed by the body and made available to the ruminant.

CELLULOSE DIGESTION IN TERMITES

Guts of wood-eating termites contain a micro-organism called Trichonympha, which secretes cellulase enzyme to digest
cellulose in wood. The termite absorbs some of the products of digestion (glucose), while Trichonympha gets sheltered.

CELLULOSE DIGESTION IN RABBITS (NON RUMINANTS)

The caecum and appendix of a rabbit contain bacteria that secrete cellulase enzyme for digesting cellulose into glucose. The
herbivore gains glucose while the bacteria get shelter.

In the process described as coprophagy (coprophagia), rabbits eat own faecal pellets while dung beetles feed on cow dung
to enable absorption of glucose at the ileum.

PARASITISM
Close relationship between organisms of different species in which one organism called parasite obtains nutrients from and
harms a larger living organism called host.
Challenges / Dangers faced by ectoparasites Challenges / Dangers faced by endoparasites

Failure to cling on the host to avoid being dislodged. Failure to penetrate the host
Failure to obtain nutritive molecules from the host. Failure to obtain nutritive molecules from the host.

Failure to find the right host for dispersal to their final host Destruction by the digestive enzymes and immune
responses of the hosts.

Complete elimination or extinction.

Fluctuating environment e.g. low oxygen tensions, excess

heat, solute concentration, darkness etc.

Failure to find the right host for dispersal to their final host

GENERAL ADAPTATIONS OF PARASITES

Structural adaptations Physiological adaptations Reproductive adaptations

Possession of penetrative devices for host Production of enzymes to digest the Some are hermaphrodites with the ability
entry e.g. fungal haustoria, cutting teeth in host’s tissues during penetration into the to carry out self fertilisation to increase the
hook worms Ancylostoma duodenale) host e.g. fungi and plasmodium rate of reproduction e.g. Fasciola, Taenia.

Possession of nutrient suckers e.g. leech Production of anticoagulants by blood Some asexually reproduce for high rate
feeding parasitic animals such as of reproduction to avoid extinction.
Development of digestive-resistant outer
mosquitoes and ticks to avoid blood
covering to avoid host’s enzyme attack e.g. Release of sexually mature forms of the
clotting during feeding.
Ascaris and Taenia etc. parasites as free living organisms e.g. in
Highly tolerant to fluctuating some parasitic animals such as the horse
Camouflaging morphology to increase hair worms
environment e.g. anaerobic respiration in
survival chances e.g. brown ticks on brown
cattle. areas of low oxygen tensions, high
Production of large number of infective
temperatures, darkness and pH changes in
agents such as eggs, cysts, and spores
Possession of specialised mouth parts in places where they live e.g. most
which increase survival chances to avoid
some ecto-parasites to suck hosts e.g. sharp endoparasites.
extinction e.g. tape worms.
stylets in aphids and tsetse flies.
Rapid means of escape which increases
Development of reproductive bodies that
Possession of specialised haustorial their chances of survival e.g. fleas and
are highly resistant when out of the host to
structures in Cuscuta (Dodder plants) for mosquitoes.
survive adverse conditions e.g. cysts in
obtaining nutrients from the host
Production of much mucus for resisting amoeba, fungal spores, etc.
Degeneration of non-essential organs e.g. digestion by host’s enzymes.
Use of intermediate host (vector) for their
no feeding organs, no locomotory organs,
Some endoparasites produce chemicals to transfer to primary host e.g. plasmodium in
no alimentary canal to reduce body size and
protect themselves against the immune female anopheles mosquito to man.
fit in intestines /blood vessels and for
response of the host.
reducing energy expenditure on such organs Some parasites localise the strategic
for example Fasciola hepatica (liver fluke), points for propagation to the next host e.g.
tape worm, hook worm etc. HIV which causes AIDS is localised in the
sex organs.

Some use hereditary transmission for

increased spreading i.e. some parasites
infect the ovary of primary host which lays
parasite infected eggs.

COMMON PARASITES
Definitive host (final host / primary host): a host in which a parasite attains sexual maturity.
 Intermediate host (secondary host): a host in which a parasite passes one or more of its asexual stages; usually designated
first and second, if there is more than one.

Phylum/division Parasite Effect on primary host

Fasciola hepatica (liver Fluke) Sheep, cattle Pond snails Liver rot
Schistosoma mansoni (blood fluke) Humans Pigs Schistosomiasis (Bilharzia)
Platyhelminthes
Taenia solium (Pork tape worm) Humans Pigs Taeniasis; Anaemia, Weight loss
Abdominal (intestinal) pain
Taenia saginata (Cattle tapeworm) Humans Cattle
Nematoda Ascaris lumbricoides (roundworm) Humans None Ascariasis, Intestinal obstruction

Spermatophyta Dodder plant (Cuscuta) Nettle, clover, None Damages tissues causing
(Seed plants) tomato, potato secondary infections
Spermatophyta Striga sp. (witch weeds) Maize, millet, None Stunted growth, wilting, and
groundnut, etc.
(Seed plants) chlorosis

Heterokontophyta Phytophthora infestans Tomato leaves None Late blight of potato and tomato
(Black leaf spots, tuber rot)

Arthropoda Plasmodiun Female Humans Malaria fever

Anopheles

Host
Primary Secondary
LIFECYCLES OF SELECTED PARASITES

Lifecycle of Ascaris lumbricoides (roundworm) Adaptations of Ascaris to parasitic life

Adult female in lumen of ileum lays about 200,000 eggs daily, Degeneration of structures reduces space
which are passed out in faeces. occupied.

Fertile eggs embryonate and become infective after about three Possession of digestive-resistant cuticle resists
destruction by the host’s enzymes.
weeks, (optimum conditions: moist, warm, shaded soil).
Ability to position itself in a habitat where it
On being swallowed by humans, eggs hatch into larvae, which gains maximum nourishment.
invade intestinal wall, and are carried via the portal, then systemic
circulation to lungs. Eggs have protective/resistant shell which is
their main ineffective and resistant stage.
Larvae mature further in lungs (10 to 14 days), penetrate alveolar
walls, ascend the bronchi to the throat, and are swallowed into gut. Tolerance to oxygen deficient environment

Upon reaching the ileum, they develop into adult worms. Ability to copulate within the intestines followed
by the laying of very many eggs increases survival
Between 2 and 3 months are required from ingestion of the infective chances.
eggs to oviposition by the adult female.

Adult worms can live 1 to 2 years.

Lifecycle of Taenia sp. (Tapeworm) Adaptations of Taenia to parasitism

Humans are the definitive hosts for T. saginata and T. solium. Has hooks and suckers for holding
tightly onto ileum wall.
Eggs or gravid proglottids are passed out in faeces;
Flattened body increases surface
Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation
area for absorbing its host’s digested
contaminated with eggs or gravid proglottids.
food
In the animal’s intestine, the oncospheres hatch, invade the intestinal wall, and
Degeneration of structures reduces
migrate to striated muscles, where they develop into cysticerci. A cysticercus can
on space occupied.
survive for several years in the animal. Humans become infected by ingesting
raw or undercooked infected meat. Lays many eggs to increase survival
chances.
In the human intestine, the cysticercus develops over 2 months into an adult
tapeworm, which can survive for years. Hooks for boring through the gut of
the host
Adult tapeworms attach and stay in small intestine by their scolex.
Eggs have a thick shell for resisting
The adults produce proglottids which mature, become gravid, detach from the
enzyme destruction.
tapeworm, and migrate to the anus or are passed in the stool (approx 6 per day).
Being hermaphrodite increases
The eggs contained in the gravid proglottids are released after the proglottids are reproductive rate
passed with the feces.

Hygienic practices for controlling endoparasites

Avoid eating infected under cooked meat

Through proper disposal of sewage which prevents these worms from spreading

Through cooking meat thoroughly for example prolonged heating destroys the tapeworm bladders
 Regular deworming to flush the worm out of the wall of the intestines in faeces.

Through regular meat inspection before it is consumed by man.

By prohibition of the discharge of raw sewage into inland waters and seas.

PLASMODIUM – THE MALARIA CAUSING PARASITE

There are approximately 156 named species of Plasmodium which infect various species of vertebrates. Four species are
considered true parasites of humans, as they utilize humans almost exclusively as a natural intermediate host: P. falciparum,

P. vivax, P. ovale and P. malariae.

LIFE CYCLE OF PLASMODIUM

Malaria parasite life cycle involves humans as intermediate host and adult female anopheles mosquito as definitive host.

During a blood meal, a malaria-infected female Anopheles mosquito releases sporozoites into human blood.

On reaching the liver, sporozoites infect liver cells and mature into schizonts, which rupture and release merozoites.

After this initial replication in the liver (exo-erythrocytic schizogony), the parasites undergo asexual multiplication in the
erythrocytes (erythrocytic schizogony).

Merozoites infect red blood cells, the ring stage trophozoites mature into schizonts, which rupture releasing merozoites.

Some parasites differentiate into sexual erythrocytic stages (gametocytes).

Blood stage parasites are responsible for the clinical manifestations of the disease.

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito
during a blood meal.

The parasites’ multiplication in the mosquito is known as the sporogonic cycle.

 While in the mosquito’s stomach, the microgametes penetrate the macrogametes-generating zygotes.

Zygotes become motile and elongated (ookinetes), invade the midgut wall of the mosquito to develop into oocysts.

Oocysts grow, rupture, and release sporozoites, which enter the mosquito’s salivary glands.

Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle.

LIFE CYCLE OF PHYTOPHTHORA INFESTANS

Phytophthora produce two kinds of spore i.e. diploid oospores, formed sexually from fusion of haploid antheridia and

oogonia, and chlamydospores formed asexually. Both types of spore have thick cell walls for surviving harsh conditions.

Under cool wet conditions, Phytophthora spores (oospores or chlamydospores) germinate to form hyphae or directly
produce sporangia.

Sporangia release free swimming biflagellated zoospores, which travel in moisture at the surface of leaves, and in soil.

On reaching plant root or leaf surface a zoospore forms a cyst.

The encysted zoospore then germinates to form hyphae on the host surface, which penetrates plant leaf or root tissues to
absorb nutrients.

After Phytophthora infects the plant, it produces sporangia and zoospores which further infect other tissues of the same
plant or nearby plants.

Sexual reproduction occurs when positive and negative mating types are present.

Haploid nuclei of antheridium and oogonium fuse together when the antheridium enters the oogonium to form a
diploid oospore, which develops into a sporangium and the cycle will continue as is would asexually.

TYPICAL EXAMINATION QUESTION

1. The blood fluke, Schistosoma mansoni is an important helminth parasite that resides within the mesenteric
veins of its definite host. Experiments were done and the graphs in figures 1, 2 and 3 below show the effect of
temperature, light and salinity on the hatching of the eggs of Schistosoma mansoni. At hourly intervals, the number of
eggs hatching was determined and expressed as a percentage of total hatch.

Figure 1 shows the effect of temperature on hatching. After 4 hours of treatment at the temperatures shown, the samples
were incubated for a further two hours at 280C at constant light and salinity.

Figure 2 shows the effect of light on hatching. One sample was kept in light for 6 hours while a second sample was first kept
in the dark for 3 hours, then transferred to light for 3 hours at constant temperature and salinity.

Figure 3 shows the effect of salinity on hatching after treatment for 6 hours at constant temperature and light (percentage of
total hatch is expressed as a % of number of eggs hatching in 0% saline).
The eggs kept in 0.8% saline for 6 hours as in figure 3 above were removed, divided equally into four lots and placed in a
range of saline solutions for a further 6 hours. The results are as shown in table 1 below:

Salinity (%) Total hatch after 6 hours (%)

0.0 100
0.2 40
0.4 20
0.6 8

PROBABLE SOLUTIONS
(a) Comment on the effect of temperature on the hatching of the eggs of Schistosoma mansoni. (7 marks)

● At constant light, salinity and temperature of 280C; ✔ eggs hatched rapidly; ✔ to completion; ✔

● At higher temperature of 370C and lower temperature of 40C; ✔hatching is just slightly stimulated (greatly inhibited); ✔

● Restoring temperature from 370C and 40C to 280C; ✔stimulates rapid hatching; ✔

(b) Explain the effect of light on the percentage of the total hatch of the eggs. (6 marks)
● The lot of eggs exposed to light hatch rapidly to completion; ✔ because light stimulates / activates a
hatching substance/enzyme; ✔ which digests/breaks down the egg membranes to enable emergence of
 larvae; ✔
● Darkness generally inhibits hatching; ✔ because the hatching substance is inactive; ✔ however in this case a little
hatching occurred in the dark probably due to experimental errors which resulted in some illumination of eggs;✔

(c) What is the effect of salinity on the percentage of total hatch of the eggs? (4 marks)
● In fresh water (at 0% salinity) all eggs hatched; ✔ at 0.8% salinity no eggs hatched (hatching was inhibited); ✔
increase in salinity; ✔ causes a rapid decrease in hatching; ✔
(d) From the data presented and restricting yourself to the egg stage only, discuss the adaptation of S.
mansoni (For more information, see MBV Roberts; functional approach, pg. 552-553)

● In the mesenteric veins of the main host of Schistosoma mansoni; ✔ there is total darkness and temperature is about 370C;

✔both of which prevent hatching of eggs into miracidia (larvae) in man; ✔because they would die; ✔

● When faeces with eggs reach fresh water bodies; ✔where there is much illumination (light), lower temperature and
very low salinity; ✔ all of which favour rapid hatching of eggs; ✔ many larvae (miracidia) are formed; ✔ which infect
water snails; ✔ (intermediate host) and form more larvae (cercariae) that infect man; ✔

(e) (i) Name the disease caused by this blood fluke to man (1 mark)
Bilharzia (Schistosomiasis); ✔
(ii) Explain how the spread of the disease can be controlled (method and its purpose = 01 mark x 4)

● Disposal of faeces in latrines/toilets to avoid their contact with fresh water bodies; ✔

● Deworming to kill adult worms in humans; ✔

● Wearing gear (boots/shoes) that shield/protect feet from larvae (cercaria) infection; ✔

● Use molluscides to kill larvae’s (miracidia) intermediate hosts (adult snails) in water; ✔

● Biological control in which some fish and ducks are introduced in water to feed on larvae /snails; ✔
(f)(i) Explain the physiological challenges facing human endo-parasites and how they are overcome
(Any 3, @ challenge – 1 mark, how overcome – 1 mark = 06 marks)
Challenge How it is overcome

● Digestion by the host’s enzymes; ✔ ● Development of thick cuticle/secretion of inhibitory substances /mucus✔

● Osmotic changes in the habitat; ✔ ● Increased chemosensitivity in order to equilibrate with host✔

● Inhibitory chemical environment; ✔ ● Secretion of anti-inhibitory substances; ✔

● Anaerobic conditions; ✔ ● Ability to respire anaerobically; ✔

● Attack by host’s immune system; ✔ ● Development of protective structures against the host’s immune attack✔

(ii) Importance of parasitic nutrition (2 marks)

● A variety of nutrients required for growth, development and body maintenance may be obtained from
one meal Less development of digestive system since most nutrients obtained are fully /partially digested.

SAPROTROPHISM (SAPROTROPHIC NUTRITION)

The process of obtaining soluble organic substances from extracellular digestion of dead or decayed organic matter.

Saprotroph: An organism that absorbs soluble nutrients from extracellular digestion of dead/decaying organic matter.

EXAMPLES OF SAPROTROPHS
(i) Saprobes: fungi like mushrooms, yeasts and moulds
(ii) Saprophytes: saprotrophic plants e.g. sugar stick, gnome plant, Indian-pipe and putrefying bacteria which
convert complex organic substances into simpler compounds e.g. Zygomonas bacterium ferments glucose producing
alcohol, lactic acid and carbon dioxide, Clostridium aceto-butylicum forms butyl alcohol from carbohydrates,
Lactobacillus converts sugars into lactic acid.

(iii) Saprophages: Animal scavengers, such as dung beetles and vultures

DESCRIPTION OF SAPROTROPHISM IN FUNGAL MOULD LIKE MUCOR/RHIZOPUS

Under suitable conditions (moisture / water, oxygen, neutral / mildly acidic pH, temperature of about 25 °C) the saprotroph
secretes different enzymes into the dead animal/plant body; proteases, lipases, carbohydrases e.g. amylase which break down
insoluble complex organic substances into simple soluble substances as follows:

-Proteases break down proteins into amino acids

-Lipases break down lipids into fatty acids and glycerol

-Carbohydrases e.g. Amylases break down starch into maltose/simple disaccharides

The end products of extra-cellular digestion such as fatty acids and glycerol, glucose, amino acids plus other nutrients
like vitamins e.g. thiamine and ions e.g. potassium, phosphorus, and magnesium are re-absorbed into the hypha through
the cell wall by endocytosis / simple diffusion / facilitated diffusion / active transport and passed on throughout the
mycelium complex to enable growth and repair.
COMPARISON OF SAPROPHYTES WITH PARASITES
Similarities
Both: (1) are heterotrophs (2) absorb soluble food (3) have simple digestive systems (4) have sexual and asexual phases in
their reproduction (5) produce large numbers of offspring.

Differences
Parasites Saprophytes IMPORTANCE OF SAPROPHYTES

Energy derived from living Energy derived from dead Recycling of materials e.g. carbon,
organisms organisms nitrogen, phosphorus

Many stages in lifecycle Usually a single adult stage, with Brewing and baking e.g. yeast
spores inclusive (Saccharomyces)

Use a variety of food sources Making antibiotics e.g. Penicillin

Very specific to their host
Simple methods of nutrition Decomposition of wastes e.g. sewage
Nutritionally highly adapted
Almost totally fungi and bacteria Production of yoghurt and cheese
Most plant and animal groups
have representatives Food source e.g. mushrooms

Most are aerobic Anaerobic and aerobic Industrial applications e.g. leather
tanning, production of vitamins, etc.