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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-43779

Lutz, T A (2010). The role of amylin in the control of energy homeostasis. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 298(6):R1475-R1484.

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Abstract

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.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2010
Deposited On:02 Feb 2011 18:02
Last Modified:01 Jan 2014 06:44
Publisher:American Physiological Society
ISSN:0363-6119
Publisher DOI:10.1152/ajpregu.00703.2009
PubMed ID:20357016
Citations:Web of Science®. Times Cited: 38
Google Scholar™
Scopus®. Citation Count: 41

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