Amylin is an important player in the control of nutrient fluxes.
Amylin reduces eating via a meal size effect by promoting meal-ending satiation. This effect seems to depend on a direct action in the area postrema (AP), which is an area rich in
amylin receptors. Subsequent to the activation of AP neurons, the neural signal is conveyed to the forebrain via relays involving the nucleus of the solitary tract (NTS) and the lateral parabrachial nucleus (
lPBN) to the lateral hypothalamic area (LHA) and other hypothalamic nuclei. While the NTS and
lPBN seem to be necessary for
amylin's eating inhibitory effect, the role of the LHA has not yet been fully investigated.
Amylin may also act as an adiposity signal. Plasma levels of
amylin are higher in obese individuals, and chronic infusion of
amylin into the brain reduces
body weight gain and adiposity; chronic infusion of an
amylin receptor antagonist into the brain increases body adiposity.
Amylin increases energy expenditure in rats; this effect occurs under various experimental conditions after peripheral and central administration. Together, these animal data, but also clinical data in humans, indicate that
amylin is a promising candidate for the treatment of
obesity; effects are most pronounced when
amylin is combined with
leptin. Finally, recent findings indicate that
amylin acts as a
neurotrophic factor in specific brain stem areas. Whether this effect may be relevant under physiological conditions requires further studies.