Document Detail


Thyroid hormone potentiates insulin signaling and attenuates hyperglycemia and insulin resistance in a mouse model of type 2 diabetes.
MedLine Citation:
PMID:  20883475     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: The thyroid hormone, triiodothyronine (T3) has many metabolic functions. Unexpectedly, exogenous T3 lowered blood glucose in db/db mice, a model of type 2 diabetes. Here, we have explored this finding and its possible mechanisms further.
EXPERIMENTAL APPROACH: db/db and lean mice were treated with T3, the phosphoinositide 3- kinase (PI3-kinase) inhibitor, LY294002, plus T3, or vehicles. Blood glucose, insulin sensitivity, levels and synthesis were measured. Effects of T3 on intracellular insulin signaling were analyzed in 3T3-L1 pre-adipocytes with Western blotting. Knock-down of the thyroid hormone receptor α1 (TRα1) in 3T3-L1 cells was achieved with an appropriate silencing RNA (siRNA).
KEY RESULTS: Single injections of T3 (7 ng·g⁻¹ i.p.) rapidly and markedly attenuated hyperglycemia. Treatment with T3 (14 ng·g⁻¹·day⁻¹, 18 days) dose-dependently attenuated blood glucose and increased insulin sensitivity in db/db mice. Higher doses of T3 (28 ng·g⁻¹·day⁻¹) reversed insulin resistance in db/db mice. T3 also increased insulin levels in plasma and the neurogenic differentiation factor (an insulin synthesis transcription factor) and insulin storage in pancreatic islets in db/db mice. These anti-diabetic effects of T3 were abolished by the PI3-kinase inhibitor (LY294002). In 3T3-L1 preadipocytes, T3 enhanced insulin-induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and activation of PI3-kinase, effects blocked by siRNA for TRα1.
CONCLUSIONS AND IMPLICATIONS: T3 potentiated insulin signaling, improved insulin sensitivity, and increased insulin synthesis, which may contribute to its anti-diabetic effects. These findings may provide new approaches to the treatment of type 2 diabetes.
Authors:
Yi Lin; Zhongjie Sun
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  British journal of pharmacology     Volume:  162     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-13     Completed Date:  2011-07-26     Revised Date:  2012-02-01    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  597-610     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
Affiliation:
Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
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MeSH Terms
Descriptor/Qualifier:
3T3-L1 Cells
Adipocytes / drug effects,  metabolism
Animals
Basic Helix-Loop-Helix Transcription Factors / genetics,  metabolism
Blood Glucose / metabolism
Blood Pressure Determination
Body Temperature / drug effects
Body Weight / drug effects
Diabetes Mellitus, Type 2 / drug therapy*,  metabolism
Disease Models, Animal
Heart Rate / drug effects
Hyperglycemia / drug therapy*,  metabolism
Hypoglycemic Agents / pharmacology*
Insulin / blood,  metabolism*,  pharmacology
Insulin Resistance*
Islets of Langerhans / drug effects,  metabolism
Male
Mice
Mice, Mutant Strains
Nerve Tissue Proteins / genetics,  metabolism
Phosphatidylinositol 3-Kinases / metabolism
Signal Transduction / drug effects*
Triiodothyronine / metabolism,  pharmacology*
Grant Support
ID/Acronym/Agency:
R01 HL-077490/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Basic Helix-Loop-Helix Transcription Factors; 0/Blood Glucose; 0/Hypoglycemic Agents; 0/Insulin; 0/Nerve Tissue Proteins; 169238-82-8/NeuroD protein; 6893-02-3/Triiodothyronine; EC 2.7.1.-/Phosphatidylinositol 3-Kinases

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


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