Amylin's best investigated function is to reduce eating via a meal size effect by promoting meal-ending satiation. This effect seems to depend on an activation of specific area postrema neurons. Brain areas that convey the neural signal to the forebrain include the nucleus of the solitary tract and the lateral parabrachial nucleus. Acute application of
amylin modulates the activity of hypothalamic areas involved in the control of eating, namely, the lateral hypothalamic area and possibly the ventromedial hypothalamic nucleus.
Amylin also interacts with other satiating signals, such as
cholecystokinin, presumably in the brainstem. Interestingly,
amylin also exhibits characteristics of adiposity signals; plasma levels of
amylin are higher in obese individuals, chronic infusion of
amylin into the brain reduces
body weight gain and adiposity, and infusion of
amylin antagonists increases adiposity. Furthermore,
amylin maintains energy expenditure at higher levels than would be expected considering its
body weight-lowering effect. However, much less is known (e.g., site of action, signaling pathways, differential activation of brain sites, and, most importantly, physiological relevance) with respect to its role as adiposity signal and regulator of energy expenditure than about its satiating action. Notwithstanding, and perhaps because
amylin resistance does not seem to be a general and prohibitive concomitant of
obesity, animal data and recent clinical data in humans indicate that
amylin is a very promising candidate for the treatment of
obesity.
Amylin seems to be particularly effective when combined with other
hormones such as
leptin.