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    Divine Intervention Episode 15 Metabolism Review B

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    Swisskelly1
    This document provides a summary of key metabolic pathways and concepts: 1) It reviews fructose and galactose metabolism, noting their relevance to diabetes. 2) It discusses glutathione and its role in reducing oxidative stress, as well as acetaminophen toxicity. 3) Key aspects of fatty acid synthesis are outlined, such as its location, feedstocks, and regulation. 4) Glycolysis is broken down in detail across multiple sections, highlighting regulation points. 5) Glucose transporters and their tissue-specific roles in uptake and kinetics are summarized.

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    Divine Intervention Episode 15 Metabolism Review B

    Uploaded by

    Swisskelly1
    27 views18 pages
    This document provides a summary of key metabolic pathways and concepts: 1) It reviews fructose and galactose metabolism, noting their relevance to diabetes. 2) It discusses glutathione and its role in reducing oxidative stress, as well as acetaminophen toxicity. 3) Key aspects of fatty acid synthesis are outlined, such as its location, feedstocks, and regulation. 4) Glycolysis is broken down in detail across multiple sections, highlighting regulation points. 5) Glucose transporters and their tissue-specific roles in uptake and kinetics are summarized.

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    Episode 15 Metabolism Review

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    Divine Intervention Episode 15 Metabolism Review b

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    This document provides a summary of key metabolic pathways and concepts: 1) It reviews fructose and galactose metabolism, noting their relevance to diabetes. 2) It discusses glutathione and its role in reducing oxidative stress, as well as acetaminophen toxicity. 3) Key aspects of fatty acid synthesis are outlined, such as its location, feedstocks, and regulation. 4) Glycolysis is broken down in detail across multiple sections, highlighting regulation points. 5) Glucose transporters and their tissue-specific roles in uptake and kinetics are summarized.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    27 views18 pages

    Divine Intervention Episode 15 Metabolism Review B

    Uploaded by

    Swisskelly1
    This document provides a summary of key metabolic pathways and concepts: 1) It reviews fructose and galactose metabolism, noting their relevance to diabetes. 2) It discusses glutathione and its role in reducing oxidative stress, as well as acetaminophen toxicity. 3) Key aspects of fatty acid synthesis are outlined, such as its location, feedstocks, and regulation. 4) Glycolysis is broken down in detail across multiple sections, highlighting regulation points. 5) Glucose transporters and their tissue-specific roles in uptake and kinetics are summarized.

    Copyright:

    © All Rights Reserved
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    of 18

    Divine Intervention Episode 15

    Metabolism Review B
    Some MS4
    Intro

    The “Central Dogma” of


    Metabolism.
    1
    How is fructose absorbed in enterocytes
    (transporter)? How can glucose be converted to
    fructose? How is this information clinically relevant
    (read diabetics)? What is the general
    pathophysiology behind lactase deficiency?
    Galactose Metabolism
    Fructose Metabolism
    Other Important Stuff
    -You should by now notice that the main job of a kinase is to
    phosphorylate stuff. “Phosphorylated stuff” cannot leave cells.
    They also tend to be osmotically active. This explains the many
    problems associated with the “2nd enzyme” in the 2 metabolic
    pathways we just discussed.

    -Note the temporal association of the diseases presented to


    breastfeeding and introduction of fruits.
    2
    Discussion of microbe destruction in lysosomes of
    macrophages after phagocytosis by the respiratory
    burst. ALS relationship. AML relationship.
    Reducing oxidative stress with Glutathione.
    Essential pathway to providing reducing power for
    cells. Treating CGD. Acetaminophen toxicity and
    rescue agent. The many “roles” of this rescue agent.
    3
    How does INH cause seizures (mechanism). The
    T1DM association. How does the urea cycle relate
    to NO synthesis? Patient with recurrent episodes of
    bronchospasm, flushing, and diarrhea presents with
    new onset memory loss and a diffuse body rash. A
    holosystolic murmur is heard at the LLSB.
    Associated valvular lesions. Common principle in
    hydroxylation reactions.
    4
    Location of FA Synthesis (FAS)? Feedstock for
    FAS? How does this feedstock leave the
    mitochondria? What is the inducement for FAS to
    begin (+ RLE of TCA cycle)? RLE of FAS. The ABC
    story. Regulation of FAS (hormonal, feedforward,
    feedback). Another HY example of feedforward
    regulation. 2 sources of NADPH for FAS (+citrate
    connection). The 2 HY essential FAs.
    5A-Glycolysis Broken Down Part 1
    5B-Glucokinase vs. Hexokinase
    -Hexokinase has a low KM and VMAX.
    -Glucokinase has a high KM and VMAX.
    Glucokinase is also induced by insulin.
    Glucokinase is regulated by a regulatory
    protein under the auspices of F-6-P and
    glucose. MODY is assoc. w/GK mutations.
    5C-Glucokinase Regulatory Protein
    -Is an inhibitor of glucokinase (GK).

    -Binds GK and sends it to the nucleus (where it is inactive).

    -GKRP has the ability to bind both F6P and glucose.

    -When bound by F6P, GKRP has a higher affinity for GK (which sequesters GK by
    taking it to the nucleus).

    -When bound by glucose, GKRP has a much lower affinity for GK (which brings it
    back to the cytoplasm for reaction).
    5D-Glycolysis Broken Down Part 2
    5E-Glycolysis Broken Down Part 3
    5F-Glycolysis Broken Down Part 4
    5G-Some Other Important Stuff
    -Pyruvate kinase is also regulated by phosphorylation and dephosphorylation.

    -Overall, glycolysis gives rise to the rule of 2s (2 ATPs, 2 NADH, and 2 Pyruvates).

    Pyruvate has multiple fates;

    -It can form lactate under the action of lactate DH. This step regenerates NAD to keep
    the Glyceraldehyde-3-P DH step working.

    -Pyruvate can go into mitochondria to receive special attention from the PDH complex
    ultimately leading to Acetyl-coA formation.

    -Pyruvate can receive special attention from Pyruvate carboxylase (what is a HY


    cofactor utilized by this enzyme???) to form OAA that can reverse course in
    gluconeogenesis (through subsequent PEPCK action).
    6A-GLUT Transporters
    6B-GLUT Transporters contd.
    -As a correlation from prior blocks, remember that GLUT1 transporters operate under
    zero order kinetics by virtue of their low KM (approx. 5 mM) which tracks along with
    normal blood glucose levels.

    -GLUT 2 transporters have a KM that is much higher than normal blood glucose
    levels. If you consider the Michaelis Menten curve, this is ideal b/c the transporters will
    operate on the “straight line” portion which essentially guarantees “proportional”
    glucose uptake that tracks along with blood glucose levels.

    -Why are GLUT2 transporters bidirectional?

    -GLUT4 transporters are insulin dependent. Muscle has the unique ability to express
    GLUT4 transporters in an “insulin independent” fashion in the setting of exercise.
    How is GLUT5 related to the reproductive system?

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