At variance with the idea of a possible relationship between LCN-2 upregulation and the
anorexigenic effects induced by the overactivity of the melanocortin 4 receptor(MC4R-) pathway [97, 98], pioglitazone treatment failed to stimulate an increase of body weight in ALS patients and in SOD1 mice [102], a lack of effect described by the hypothesis of defective melanocortin system and downregulation of proopiomelanocortin (POMC) neurons in ALS.
Despite the fact that [alpha]-MSH is an
anorexigenic neuropeptide, as mentioned above, many studies on adults have demonstrated that obese subjects had higher levels of [alpha]-MSH than do normal-weight or lean subjects.
Reduced food intake is associated with reduced gastric emptying, so it is consistent with the
anorexigenic role of NmU that i.c.v.
The production of leptin could be responsible for the
anorexigenic effect.
Individuals were not eligible if they were currently using fiber supplements or had intolerance to fiber supplements, had untreated/unstable metabolic conditions known to influence weight status (e.g., hypothyroidism, type 2 diabetes mellitus), had gastrointestinal disorders that might cause complications or influence motility or satiety (e.g., diverticulitis, inflammatory bowel disease, irritable bowel syndrome, intestinal narrowing or obstruction, and difficulty swallowing), were using medications or complementary and alternative medicine (CAM) therapies that might affect weight or food absorption (e.g., diuretics, glucocorticoids,
anorexigenic agents, Orlistat, acupuncture, and Hoodia), had an eating disorder, or were participating in a weight loss program.
Following a meal, centrally acting insulin exerts
anorexigenic effects in the hypothalamus via stimulation of proopiomelanocortin (POMC) and inhibition of NYP neurons.
Ghrelin is an orexigenic hormone that has an opposing effect to the
anorexigenic properties of leptin.
Leptin receptor on the hypothalamus colocalizes with ERalpha and estrogen treatment decreases the expression of leptin receptor on the arcuate nucleus, where leptin exerts its catabolic actions being
anorexigenic and increasing energy expenditure.
Several excellent reviews on the topic have recently been published (38, 39), with the balance of data supporting several critical metabolic functions including (a)
anorexigenic action via central nervous system control of feeding behavior, (b) augmented glucose disposal in skeletal muscle via actions on several proteins in the insulin signaling pathway and by increased glucose transporter type 4 translocation, (c) prevention of visceral fat accumulation and decreased lipogenic activity of lipoprotein lipase in adipose tissue, and (d) antiapoptotic effects on pancreatic [beta]-cells.
AMPK is also affected by several orexigenic and
anorexigenic signals in the hypothalamus (e.g.
IIP induces body weight reduction due to the
anorexigenic effect of GLP-1.