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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-43774

Lutz, T A (2011). Steve Woods's contribution to research on amylin's eating inhibitory effect. Physiology & Behavior, 103(1):25-30.

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Abstract

Amylin is secreted by pancreatic beta-cells and seems to function as a physiological signal of satiation and possibly also as an adiposity signal. Amylin's satiating effect is mediated via a direct action at area postrema (AP) neurons. The central pathways mediating amylin's effects rely on connections from the AP to the nucleus of the solitary tract and lateral parabrachial nucleus. Amylin was shown to interact, probably at the brainstem, with other satiating signals, namely cholecystokinin, glucagon-like peptide 1 and peptide YY, and other adiposity signals, namely leptin and insulin. The interaction with leptin, which is thought to involve the hypothalamus, may have important implications for the development of new and improved hormonal anti-obesity treatments. Steve Woods has contributed to the recent literature on amylin's eating inhibitory effect by some frequently cited publications. Steve's work concentrated more on the central administration of amylin and on amylin's potential role as an adiposity signal. His work will be reviewed here and discussed in the context of other important findings on amylin's role in the control of energy homeostasis.

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
Date:2011
Deposited On:27 Jan 2011 17:21
Last Modified:28 Nov 2013 02:18
Publisher:Elsevier
ISSN:0031-9384
Publisher DOI:10.1016/j.physbeh.2010.10.016
PubMed ID:21035478
Citations:Web of Science®
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