Peripheral signals and food intake control

Abstract

The food intake and satiety signals are regulated by a complex metabolic net that includes nervous system and several hormones. The metabolic signals derived in the periphery determines the food intake and energy expenditure. At the end of this route, eating signals are integrated at the Central Nervous System (CNS), being the arcuate nucleus a critical partner in this regulation. Central and peripheral hunger-satiety modulators are released to promote or inhibit food intake. Of the first group, ghrelin, mainly secreted by the oxyntic X/A cells of the stomach, exerts its effects through the growth hormone secretagogue receptor 1a (GHS-R1a), stimulating food intake. This hormone is the only known peripheral orexigenic peptide. Among the satiety signals, gut hormones such as cholecystokinin (CCK), glucose-dependent insulino-tropic polypeptide (GIP), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY) are secreted depending on the type of meal and the proportions of the macronutrients. Meanwhile, the enteric nervous system (ENS) controls most of the functions of the gastrointestinal tract. When the bolus enters the stomach and the small intestine, sensory stretch receptors are activated, which, through an action potential in the receiver, transmitted via the vagus nerve to the nucleus of the solitary tract, causes relay to the ventromedial nucleous (VMN) to generate the satiety response. Furthermore, one can identify immediate and log-lasting satiety signals. In this brief assay we show the principal mechanisms of the satiety signals, and some of them have more than one mechanism and/or time of action.