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Evidence that amylin stimulates lipolysis in vivo: a possible mediator of induced insulin resistance

Citation

Ye, JM and Lim-Fraser, M and Cooney, GJ and Cooper, GJ and Iglesias, MA and Watson, DG and Choong, B and Kraegen, EW, Evidence that amylin stimulates lipolysis in vivo: a possible mediator of induced insulin resistance, American Journal of Physiology: Endocrinology and Metabolism, 280, (4) pp. E562-E569. ISSN 0193-1849 (2001) [Refereed Article]

Copyright Statement

Copyright 2001 the American Physiological Society

Official URL: http://ajpendo.physiology.org/content/280/4/E562.a...

DOI: doi:10.1152/ajpendo.2001.280.4.E562

Abstract

The present study investigated the role of amylin in lipid metabolism and its possible implications for insulin resistance. In 5- to 7-h-fasted conscious rats, infusion of rat amylin (5 nmol/h for 4 h) elevated plasma glucose, lactate, and insulin (P <0.05 vs. control, repeated-measures ANOVA) with peak values occurring within 60 min. Despite the insulin rise, plasma nonesterified fatty acids (NEFA) and glycerol were also elevated (P < 0.001 vs. control), and these elevations (80% above basal) were sustained over the 4-h infusion period. Although unaltered in plasma, triglyceride content in liver was increased by 28% (P < 0.001) with a similar tendency in muscle (18%, P = 0.1). Infusion of the rat amylin antagonist amylin-(8-37) (125 nmol/h) induced opposite basal plasma changes to amylin, i.e., lowered plasma NEFA, glycerol, glucose, and insulin levels (all P < 0.05 vs. control); additionally, amylin-(8-37) blocked amylin-induced elevations of these parameters (P < 0.01). Treatment with acipimox (10 mg/kg), an anti-lipolytic agent, before or after amylin infusion blocked amylin's effects on plasma NEFA, glycerol, and insulin but not on glucose and lactate. We conclude that amylin could exert a lipolytic-like action in vivo that is blocked by and is opposite to effects of its antagonist amylin-(8-37). Further studies are warranted to examine the physiological implications of lipid mobilization for amylin-induced insulin resistance.

Item Details

Item Type:Refereed Article
Keywords:amylin antagonist, fatty acids, glucose, acipimox
Research Division:Medical and Health Sciences
Research Group:Medical Biochemistry and Metabolomics
Research Field:Metabolic Medicine
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Diabetes
Author:Iglesias, MA (Dr Miguel Iglesias)
ID Code:80270
Year Published:2001
Web of Science® Times Cited:19
Deposited By:Health Sciences A
Deposited On:2012-10-25
Last Modified:2013-05-10
Downloads:0

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