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 , 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
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.
Leptin is a peptide hormone with a molecular structure similar to interleukins, composed of 146 amino acids, its synthesis is primarily in adipocytes, and it travels through the circulation to reach the CNS, where it interacts with the leptin receptor (LepR) located in hypothalamic neurons and regulates food intake through an anorexigenic
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.