<prompt> Which of the following hormone is related to appetite and satiety?LeptinPeptide YYPYYGhrelinAll of the above.  <response>: Ans. D. All of the above. Ref. H-17thpg. 255, 2557, 464; Fig. 74-2; Guyton 11thpg. 870; Fig. 71-1Activation of the POMC neurons decreases food intake and increases energy expenditure, whereas activation of the NPY-AGRP neurons increases food intake and reduces energy expenditure, these neurons are major targets for the actions of several hormones that regulate appetite, including leptin, insulin, CCK, and ghrelin.There are two distinct types of neurons in the arcuate nuclei of the hypothalamus that are especially important as controllers of both appetite and energy expenditure: 1 pro-opiomelanocortin POMC neurons that produce a-melanocyte-stimulating hormone a-MSH together with cocaine- and amphetamine-related transcript CART, and 2 neurons that produce the orexigenic substances neuropeptide Y NPY and agouti-related protein AGRP.NT and hormones influencing feeding and satiety centres in hypothalamusAnorexingenic decrease feedingOrexigenic increase feeding Alpha-MSH Neuropeptide Y NPY Leptin Agouti-related protein AGRP Serotonin Melanin-concentrating hormone MCH Norepinephrine Orexins A and B CRH Endorphins Insulin Galanin GAL CCK Amino acids glutamate GABA Glucagon like ppetide Cortisol Cocaine and amphetamine regulatd transcript CART Ghrelin Peptide YYPYY Ghrelin Ghrelin is a hormone released mainly by the oxyntic cells of the stomach but also, to a much less extent, by the intestine. Blood levels of ghrelin rise during fasting, peak just before eating, and then fall rapidly after a meal, suggesting a possible role in stimulating feeding. Also, administration of ghrelin increases food intake in experimental animals, further supporting the possibility that it may be an orexigenic hormone.Leptin: hypothalamus senses energy storage through the actions of leptin, a peptide hormone released from adipocytes. Leptin circulates to the brain, where it moves across the BBB by facilitated diffusion and occupies leptin receptors at multiple sites in the hypothalamus, especially the POMC neurons of the arcuate nuclei and neurons of the paraventricular nuclei. Stimulation of leptin receptors in these hypothalamic nuclei initiates multiple actions that decrease fat storage, including: l.decreased production in the hypothalamus of appetite stimulators, such as NPY and AGRP; 2 activation of POMC neurons, causing release of a-MSH and activation of melanocortin receptors; 3 increased production in the hypothalamus of substances, such as corticotropin-releasing hormone, that decrease food intake; 4 increased sympathetic nerve activity through neural projections from the hypothalamus to the vasomotor centers, which increases metabolic rate and energy expenditure; and 5 decreased insulin secretion by the pancreatic beta cells, which decreases energy storage. Thus. leptin mav be an important means bv which the adipose tissue signals the brain that enough energy has been stored and that intake of food is no longer necessary.Peptide YYPYY Peptide YY PYY is secreted from the entire GIT, but especially from the ileum and colon. Food intake stimulates release of PYY, with blood concentrations rising to peak levels 1 to 2 hours after ingesting a meal. These peak levels of PYY are influenced by the number of calories ingested and the composition of the food, with higher levels of PYY observed after meals with a high fat content. Although injections of PYY into mice have been shown to decrease food intake for 12 hours or more, the importance of this Gl hormone in regulating appetite in humans is still unclear. Agentse.g.ActionNeuropeptidesCorticotropin-releasing hormone CRH,a-melanocyte- stimulating hormone ot-MSH, and cocaine- and amphetamine- related transcript CARTInduce anorexia by acting centrally on satiety centers.Gl peptidesGhrelin,Glucagon,Somatostatin, andCholecystokininSignal satiety and thus decrease food intake.InsulinHypoglycemiaHypoglycemia suppresses insulin, reducing glucose utilization and inhib-iting the satiety center. 