What are the mechanisms for satiety?

Question

What will be an ideal response?

Answer 1

Satiety, or fullness, occurs long before sufficient nutrients make their way into cells. Stomach fullness provides an early warning signal to tell us that we have eaten enough. The intestines also provide satiety signals. The duodenum joins the stomach and the small intestines. When duodenal glucoreceptors sense sugars, eating generally stops quickly. The arrival of foods containing fats and proteins at the duodenum signals the release of the peptide CCK. CCK promotes the release of insulin by the pancreas and contracts the gallbladder to release bile to help break down fats. CCK clearly contributes to feelings of satiety. Early research suggested that the VMH might serve as a satiety center. Lesions of the VMH in rats produced VMH syndrome, characterized by large weight gains and picky eating habits. However, it is overly simplistic to view the VMH as a single center for satiety. Animals with VMH lesions do not continue to eat indefinitely. Instead they seem to establish a much higher set point, which is then defended in a somewhat normal manner. Lesions of the VMH not only destroy the VMH nucleus itself but also damage important adjacent fiber pathways. Among these pathways are fibers connecting the PVN to the NST in the brainstem. The NST receives information from glucoreceptors and taste receptors and participates in energy storage. Disruption of this pathway could easily produce abnormal eating patterns. VMH lesions also result in excess insulin production.