Document Detail


GLP-1 treatment reduces endogenous insulin resistance via activation of central GLP-1 receptors in mice fed a high-fat diet.
MedLine Citation:
PMID:  20530733     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glucagon-like peptide-1 (GLP-1) improves insulin sensitivity in humans and rodents. It is currently unknown to what extent the (metabolic) effects of GLP-1 treatment are mediated by central GLP-1 receptors. We studied the impact of central GLP-1 receptor (GLP-1R) antagonism on the metabolic effects of peripheral GLP-1 administration in mice. High-fat-fed insulin-resistant C57Bl/6 mice were treated with continuous subcutaneous infusion of GLP-1 or saline (PBS) for 2 wk, whereas the GLP-1R antagonist exendin-9 (EX-9) and cerebrospinal fluid (CSF) were simultaneously infused in the left lateral cerebral ventricle (icv). Glucose and glycerol turnover were determined during a hyperinsulinemic euglycemic clamp. VLDL-triglyceride (VLDL-TG) production was determined in hyperinsulinemic conditions. Our data show that the rate of glucose infusion necessary to maintain euglycemia was significantly increased by GLP-1. Simultaneous icv infusion of EX-9 diminished this effect by 62%. The capacities of insulin to stimulate glucose disposal and inhibit glucose production were reinforced by GLP-1. Simultaneous icv infusion of EX-9 significantly diminished the latter effect. Central GLP-1R antagonism alone did not affect glucose metabolism. Also, GLP-1 treatment reinforced the inhibitory action of insulin on VLDL-TG production. In conclusion, peripheral administration of GLP-1 reinforces the ability of insulin to suppress endogenous glucose and VLDL-TG production (but not lipolysis) and boosts its capacity to stimulate glucose disposal in high-fat-fed C57Bl/6 mice. Activation of central GLP-1Rs contributes substantially to the inhibition of endogenous glucose production by GLP-1 treatment in this animal model.
Authors:
Edwin T Parlevliet; Judith E de Leeuw van Weenen; Johannes A Romijn; Hanno Pijl
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-08
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  299     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-09     Completed Date:  2010-07-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E318-24     Citation Subset:  IM    
Affiliation:
Department of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Body Weight / drug effects,  physiology
Cerebral Ventricle Neoplasms
Dietary Fats / pharmacology*
Fatty Acids, Nonesterified / blood
Glucagon-Like Peptide 1 / pharmacology*
Glucose / metabolism
Glucose Clamp Technique
Hyperinsulinism / metabolism
Insulin / blood
Insulin Resistance / physiology*
Lipoproteins, VLDL / biosynthesis
Male
Mice
Mice, Inbred C57BL
Receptors, Glucagon / antagonists & inhibitors,  drug effects*
Triglycerides / biosynthesis
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Dietary Fats; 0/Fatty Acids, Nonesterified; 0/Lipoproteins, VLDL; 0/Receptors, Glucagon; 0/Triglycerides; 0/glucagon-like peptide receptor; 11061-68-0/Insulin; 50-99-7/Glucose; 89750-14-1/Glucagon-Like Peptide 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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