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Effects of amylin on eating and adiposity


Lutz, T A (2012). Effects of amylin on eating and adiposity. In: Joost, H G. Appetite Control. Berlin, Heidelberg: Springer, 231-250.

Abstract

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.

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.

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Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:30 Mar 2012 07:36
Last Modified:05 Apr 2016 15:27
Publisher:Springer
Series Name:Handbook of Experimental Pharmacology
Number:209
ISSN:0171-2004
ISBN:978-3-642-24715-6
Publisher DOI:https://doi.org/10.1007/978-3-642-24716-3_10
Related URLs:http://opac.nebis.ch/F/?local_base=NEBIS&CON_LNG=GER&func=find-b&find_code=SYS&request=007056530
PubMed ID:22249817
Permanent URL: https://doi.org/10.5167/uzh-56267

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