Summary Episodic and Tonic Factors in the Regulation of Appetite

Endogenous 5-HT and leptin represent two aspects of negative feedback integral to the appetite control

Figure 3 The integration of peripherally generated episodic and tonic signals critical to the expression of appetite. Signals generated by both meal consumption and fat deposition are integrated into a complex hypothalamic system of neuropeptides, which in turn either stimulate or inhibit subsequent food intake. Abbreviations: 5-HT, serotonin; aMSH, alpha melanocortin stimulating hormone; AgRP, agouti-related peptide; A-IV, apoliproprotein-IV; ARC, arcuate nucleus; CART, cocaine and amphetamine-regulated transcript; CCK, cholecystokinin; CRF, corticotropin releasing factor; GAL, galanin; GLP-1, glucagon-like peptide-1; GRP, gastric releasing peptide; LH, lateral hypothalamus; MC, melanocortin; NPY, neuropeptide Y; OX, orexin; PVN, paraventricular hypothalamus; POMC, pre-pro-opiomelanocortin; PYY, peptide YY.

Figure 3 The integration of peripherally generated episodic and tonic signals critical to the expression of appetite. Signals generated by both meal consumption and fat deposition are integrated into a complex hypothalamic system of neuropeptides, which in turn either stimulate or inhibit subsequent food intake. Abbreviations: 5-HT, serotonin; aMSH, alpha melanocortin stimulating hormone; AgRP, agouti-related peptide; A-IV, apoliproprotein-IV; ARC, arcuate nucleus; CART, cocaine and amphetamine-regulated transcript; CCK, cholecystokinin; CRF, corticotropin releasing factor; GAL, galanin; GLP-1, glucagon-like peptide-1; GRP, gastric releasing peptide; LH, lateral hypothalamus; MC, melanocortin; NPY, neuropeptide Y; OX, orexin; PVN, paraventricular hypothalamus; POMC, pre-pro-opiomelanocortin; PYY, peptide YY.

system (see Figure 3). Both systems appear to inhibit NPY functioning, the effect of leptin being partly mediated by melanocortins and other excitatory and inhibitory neuropeptides. 5-HT mediates the effect of meal-derived satiety factors derived from pre- and postingestive processes (such as CCK and enterostatin relsease) and promotes meal termination, prolonging the intermeal interval. By such a mechanism the body deals with the daily physiological fluxes that result from meal intake ensuring an approximately appropriate daily energy intake. Circulating leptin accurately reflects the current status of the body's energy store. Leptin levels continually modify total daily and meal food intake to maintain a sufficient but not excessive level of energy deposition. Thus, 5-HT and leptin represent two classes of signals: short-term episodic and long-term tonic feedback, respectively. The net result of the action both episodic and tonic signals will be an adjustment in the expression of appetite, adjusting subsequent feeding behavior to compensate for previous intake and energy stored.

See also: Appetite: Psychobiological and Behavioral Aspects. Brain and Nervous System. Hunger. Lipoproteins.

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