Document Detail

Calpain inhibition and insulin action in cultured human muscle cells.
MedLine Citation:
PMID:  15862281     Owner:  NLM     Status:  MEDLINE    
Variation in the calpain 10 gene has been reported to increase susceptibility to type 2 diabetes. Part of this susceptibility appears to be mediated by a decrease in whole body insulin sensitivity. As skeletal muscle is the primary tissue site of the peripheral insulin resistance in type 2 diabetes, the aim of this study was to use a human skeletal muscle cell culture system to explore the effects of calpain inhibition on insulin action. Calpain 10 mRNA and protein expression was examined in cultured myoblasts, myotubes, and whole skeletal muscle from non-diabetic subjects using RT-PCR and Western blotting. Changes in insulin-stimulated glucose uptake and glycogen synthesis in response to the calpain inhibitors ALLN and ALLM were measured. Calpain 10 expression was confirmed in cultured human myoblasts, myotubes, and native skeletal muscle. Insulin-stimulated glucose uptake was significantly decreased following preincubation with ALLN [404+/-40 vs 505+/-55 (mean+/-SEM)pmol/mg/min; with vs without ALLN: p = 0.04] and ALLM [455+/-38 vs 550+/-50 pmol/mg/min; with vs without ALLM: p = 0.025] in day 7 fused myotubes, but not in myoblasts. Neither ALLN nor ALLM affected insulin-stimulated glycogen synthesis in myoblasts or myotubes. These studies confirm calpain 10 expression in cultured human muscle cells and support a role for calpains in insulin-stimulated glucose uptake in human skeletal muscle cells that may be relevant to the pathogenesis of the peripheral insulin resistance in type 2 diabetes.
L J Logie; A E Brown; S J Yeaman; M Walker
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-02-16
Journal Detail:
Title:  Molecular genetics and metabolism     Volume:  85     ISSN:  1096-7192     ISO Abbreviation:  Mol. Genet. Metab.     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-05-02     Completed Date:  2005-09-26     Revised Date:  2007-08-13    
Medline Journal Info:
Nlm Unique ID:  9805456     Medline TA:  Mol Genet Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  54-60     Citation Subset:  IM    
School of Clinical Medical Sciences, University of Newcastle upon Tyne, Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
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MeSH Terms
Base Sequence
Biological Transport
Calpain / antagonists & inhibitors*,  genetics*
Cell Culture Techniques
Cells, Cultured
DNA Primers
Diabetes Mellitus, Type 2 / genetics*
Gene Expression Regulation, Enzymologic
Genetic Predisposition to Disease
Glucose / metabolism
Glycogen / biosynthesis
Insulin / pharmacology
Insulin Resistance / genetics
Muscle, Skeletal / drug effects,  physiology*
RNA, Messenger / genetics
Reverse Transcriptase Polymerase Chain Reaction
Transcription, Genetic
Grant Support
//Wellcome Trust
Reg. No./Substance:
0/DNA Primers; 0/RNA, Messenger; 11061-68-0/Insulin; 50-99-7/Glucose; 9005-79-2/Glycogen; EC 3.4.22.-/Calpain; EC 3.4.22.-/calpain 10

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

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