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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 |
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Keywords: | amylin antagonist, fatty acids, glucose, acipimox |
Research Division: | Biomedical and Clinical Sciences |
Research Group: | Medical biochemistry and metabolomics |
Research Field: | Metabolic medicine |
Objective Division: | Health |
Objective Group: | Clinical health |
Objective Field: | Clinical health not elsewhere classified |
UTAS Author: | Iglesias, MA (Dr Miguel Iglesias) |
ID Code: | 80270 |
Year Published: | 2001 |
Web of Science® Times Cited: | 21 |
Deposited By: | Health Sciences A |
Deposited On: | 2012-10-25 |
Last Modified: | 2013-05-10 |
Downloads: | 0 |
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