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The roles of amylin in satiation, adiposity and brain development


Lutz, T A (2009). The roles of amylin in satiation, adiposity and brain development. In: Langhans, W; Geary, N. Frontiers in Eating and Weight Regulation. Forum Nutrition: Karger, 64-74.

Abstract

Amylin plays an important role in the control of nutrient fluxes. It is cosecreted with insulin and reduces eating by promoting meal-ending satiation. This effect seems to depend on a stimulation of amylin receptors in the area postrema (AP). Subsequent to AP activation, the neural signal is conveyed to the forebrain via distinct relays in the nucleus of the solitary tract (NTS) and the lateral parabrachial nucleus (lPBN) to the lateral hypothalamic area (LHA) and other hypothalamic nuclei; the functional roles of these relays in amylin’s eating inhibitory effect have not been fully investigated. Amylin may also play a role in the regulation of adiposity. Plasma levels of amylin are increased in adiposity, although the precise relation is unknown. Furthermore, chronic infusion of amylin into the brain reduced body weight gain and adiposity, and chronic infusion of an amylin receptor antagonist increased body adiposity. Both these animal data and pre-clinical research in humans indicate that amylin is a promising option for anti-obesity therapy, especially in combination with leptin. Finally, recent findings indicate that amylin may also be necessary for normal brain development; it acts as a neurotrophic factor for the development of brainstem pathways involved in the control of eating. How this may be relevant under physiological conditions requires further studies, but these findings substantiate the concept that amylin plays an integrative role in the development and operation of neural circuits involved in the control of eating and energy homeostasis.

Abstract

Amylin plays an important role in the control of nutrient fluxes. It is cosecreted with insulin and reduces eating by promoting meal-ending satiation. This effect seems to depend on a stimulation of amylin receptors in the area postrema (AP). Subsequent to AP activation, the neural signal is conveyed to the forebrain via distinct relays in the nucleus of the solitary tract (NTS) and the lateral parabrachial nucleus (lPBN) to the lateral hypothalamic area (LHA) and other hypothalamic nuclei; the functional roles of these relays in amylin’s eating inhibitory effect have not been fully investigated. Amylin may also play a role in the regulation of adiposity. Plasma levels of amylin are increased in adiposity, although the precise relation is unknown. Furthermore, chronic infusion of amylin into the brain reduced body weight gain and adiposity, and chronic infusion of an amylin receptor antagonist increased body adiposity. Both these animal data and pre-clinical research in humans indicate that amylin is a promising option for anti-obesity therapy, especially in combination with leptin. Finally, recent findings indicate that amylin may also be necessary for normal brain development; it acts as a neurotrophic factor for the development of brainstem pathways involved in the control of eating. How this may be relevant under physiological conditions requires further studies, but these findings substantiate the concept that amylin plays an integrative role in the development and operation of neural circuits involved in the control of eating and energy homeostasis.

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16 citations in Web of Science®
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Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Physiology
04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2009
Deposited On:23 Nov 2009 14:18
Last Modified:21 Aug 2016 05:04
Publisher:Karger
Series Name:Forum of Nutrition
Number:63
ISSN:0067-8198
ISBN:978-3-8055-9300-7
Related URLs:http://www.recherche-portal.ch/ZAD:default_scope:ebi01_prod005938151 (Library Catalogue)

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