Amylin is an important control of nutrient fluxes because it reduces energy intake, modulates nutrient utilization by inhibiting postprandial
glucagon secretion, and increases energy disposal by preventing compensatory decreases of energy expenditure in weight-reduced individuals. The best investigated function of
amylin which is cosecreted with
insulin is to reduce eating by promoting meal-ending satiation. This effect is thought to be mediated by a stimulation of specific
amylin receptors in the area postrema. Secondary brain sites to mediate
amylin action include the nucleus of the solitary tract and the lateral parabrachial nucleus, which convey the neural signal to the lateral hypothalamic area and other hypothalamic nuclei.
Amylin may also signal adiposity because plasma levels of
amylin are increased in adiposity and because higher
amylin concentrations in the brain result in reduced
body weight gain and adiposity, while
amylin receptor antagonists increase body adiposity. The central mechanisms involved in
amylin's effect on energy expenditure are much less known. A series of recent experiments in animals and humans indicate that
amylin is a promising option for anti-
obesity therapy especially in combination with other
hormones. The most extensive dataset is available for the combination
therapy of
amylin and
leptin. Ongoing research focuses on the mechanisms of these interactions.