Document Detail


Increased collagen content in insulin-resistant skeletal muscle.
MedLine Citation:
PMID:  16249255     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oversupply and underutilization of lipid fuels are widely recognized to be strongly associated with insulin resistance in skeletal muscle. Recent attention has focused on the mechanisms underlying this effect, and defects in mitochondrial function have emerged as a potential player in this scheme. Because evidence indicates that lipid oversupply can produce abnormalities in extracellular matrix composition and matrix changes can affect the function of mitochondria, the present study was undertaken to determine whether muscle from insulin-resistant, nondiabetic obese subjects and patients with type 2 diabetes mellitus had increased collagen content. Compared with lean control subjects, obese and type 2 diabetic subjects had reduced muscle glucose uptake (P<0.01) and decreased insulin stimulation of tyrosine phosphorylation of insulin receptor substrate-1 and its ability to associate with phosphatidylinositol 3-kinase (P<0.01 and P<.05). Because it was assayed by total hydroxyproline content, collagen abundance was increased in muscle from not only type 2 diabetic patients but also nondiabetic obese subjects (0.26+/-0.05, 0.57+/-0.18, and 0.67+/- 0.20 microg/mg muscle wet wt, lean controls, obese nondiabetics, and type 2 diabetics, respectively), indicating that hyperglycemia itself could not be responsible for this effect. Immunofluorescence staining of muscle biopsies indicated that there was increased abundance of types I and III collagen. We conclude that changes in the composition of the extracellular matrix are a general characteristic of insulin-resistant muscle.
Authors:
Rachele Berria; Lishan Wang; Dawn K Richardson; Jean Finlayson; Renata Belfort; Thongchai Pratipanawatr; Elena A De Filippis; Sangeeta Kashyap; Lawrence J Mandarino
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2005-10-25
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  290     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-02-09     Completed Date:  2006-03-23     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E560-5     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Biopsy
Collagen Type I / metabolism*
Collagen Type III / metabolism*
Diabetes Mellitus, Type 2 / metabolism
Extracellular Matrix / metabolism*
Female
Glucose / metabolism,  pharmacology
Humans
Hydroxyproline / metabolism
Insulin / pharmacology
Insulin Receptor Substrate Proteins
Insulin Resistance / physiology
Male
Microscopy, Fluorescence
Middle Aged
Muscle, Skeletal / metabolism*
Obesity / metabolism
Phosphoproteins / metabolism
Phosphorylation
Tyrosine / metabolism
Grant Support
ID/Acronym/Agency:
M01-RR-01346/RR/NCRR NIH HHS; R01-DK-47936/DK/NIDDK NIH HHS; R01-DK-66938/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Collagen Type I; 0/Collagen Type III; 0/IRS1 protein, human; 0/Insulin Receptor Substrate Proteins; 0/Phosphoproteins; 11061-68-0/Insulin; 50-99-7/Glucose; 51-35-4/Hydroxyproline; 55520-40-6/Tyrosine

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


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