Document Detail


Hyperinsulinemia precedes insulin resistance in mice lacking pancreatic beta-cell leptin signaling.
MedLine Citation:
PMID:  20631001     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The adipocyte hormone leptin acts centrally and peripherally to regulate body weight and glucose homeostasis. The pancreatic beta-cell has been shown to be a key peripheral target of leptin, with leptin suppressing insulin synthesis and secretion from beta-cells both in vitro and in vivo. Mice with disrupted leptin signaling in beta-cells (lepr(flox/flox) RIPcre tg+ mice) display hyperinsulinemia, insulin resistance, glucose intolerance, obesity, and reduced fasting blood glucose. We hypothesized that hyperinsulinemia precedes the development of insulin resistance and increased adiposity in these mice with a defective adipoinsular axis. To determine the primary defect after impaired beta-cell leptin signaling, we treated lepr(flox/flox) RIPcre tg+ mice with the insulin sensitizer metformin or the insulin-lowering agent diazoxide with the rationale that pharmacological improvement of the primary defect would alleviate the secondary symptoms. We show that improving insulin sensitivity with metformin does not normalize hyperinsulinemia, whereas lowering insulin levels with diazoxide improves insulin sensitivity. Taken together, these results suggest that hyperinsulinemia precedes insulin resistance in beta-cell leptin receptor-deficient mice, with insulin resistance developing as a secondary consequence of excessive insulin secretion. Therefore, pancreatic beta-cell leptin receptor-deficient mice may represent a model of obesity-associated insulin resistance that is initiated by hyperinsulinemia.
Authors:
Sarah L Gray; Christine Donald; Arif Jetha; Scott D Covey; Timothy J Kieffer
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-14
Journal Detail:
Title:  Endocrinology     Volume:  151     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-25     Completed Date:  2010-10-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4178-86     Citation Subset:  AIM; IM    
Affiliation:
Laboratory of Molecular and Cellular Medicine, Department of Cellular and Physiological Sciences, Life Sciences Institute, 2350 Health Sciences Mall, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.
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MeSH Terms
Descriptor/Qualifier:
Adiposity / drug effects
Animals
Blood Glucose / metabolism
Body Weight / drug effects
Diazoxide / pharmacology
Eating / drug effects
Female
Hyperinsulinism / blood,  genetics,  physiopathology*
Hypoglycemic Agents / pharmacology
Insulin / blood
Insulin Resistance / genetics,  physiology*
Insulin-Secreting Cells / metabolism*
Male
Metformin / pharmacology
Mice
Mice, Knockout
Receptors, Leptin / deficiency,  genetics,  physiology*
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Hypoglycemic Agents; 0/Receptors, Leptin; 0/leptin receptor, mouse; 11061-68-0/Insulin; 364-98-7/Diazoxide; 657-24-9/Metformin

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


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