Explain how the short-term mechanisms that control the termination of a meal differ from the long-term mechanisms that control termination of a meal.

Question

What will be an ideal response?

Answer 1

Initially, stretch receptors in the stomach respond to increased volume as food or liquid enters the stomach and send signals to the NST of the medulla via the vagus nerve. Intake of specific nutrients is monitored by several different peptides released by the stomach and intestine that signal the brain through the vagus nerve or the bloodstream. Cholecystokinin (CCK) is one of those peptides involved in short-term control of meal termination. CCK is released by the duodenum when food enters there, and it sends signals to reduce eating to the NST and hypothalamus via the vagus nerve. The intestines also release peptides that are involved in long-term control of meal termination. One such long-term control is peptide YY3-36 (PYY), which reduces food intake over 12 hours following a meal. PYY reaches the brain more slowly than CCK because it travels through the bloodstream to the arcuate nucleus of the hypothalamus and then inhibits NPY-releasing neurons. The body's fat stores also provide long-term control over meal termination by releasing the hormone leptin. More leptin is released when fat stores are high, and this results in inhibition of NPY/AgRP neurons and activation of POMC neurons in the arcuate nucleus. The POMC neurons then inhibit neurons in the PVN and lateral hypothalamus, which reduces eating. The hormone insulin works similarly to leptin in that greater amounts are released when fat stores are high, and this reduces eating via the arcuate nucleus, PVN, and lateral hypothalamus.