Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Impaired Mitochondrial Function and Insulin Resistance of Skeletal Muscle in Mitochondrial Diabetes

Szendroedi, Julia ; Schmid, Albrecht Ingo ; Meyerspeer, Martin ; Cervin, Camilla LU ; Kacerovsky, Michaela ; Smekal, Gerhard ; Graeser-Lang, Sabine ; Groop, Leif LU and Roden, Michael (2009) 68th Annual Meeting of the American-Diabetes-Association 32(4). p.677-679
Abstract
OBJECTIVE - Impaired muscular mitochondrial function is related to common insulin resistance in type 2 diabetes. Mitochondrial diseases frequently lead to diabetes, which is mostly attributed to defective beta-cell mitochondria and secretion. RESEARCH DESIGN AND METHODS - We assessed muscular mitochondrial function and lipid deposition in liver (hepatocellular lipids [HCLs]) and muscle (intramyocellular lipids [IMCLs]) using P-31/H-1 magnetic resonance spectroscopy and insulin sensitivity and endogenous glucose production (EGP) using hyperinsulinemic-euglycemic clamps combined with isotopic tracer dilution in one female patient suffering from MELAS(myopathy,encephalopathy, lactic acidosis, and stroke-like episodes) syndrome and in six... (More)
OBJECTIVE - Impaired muscular mitochondrial function is related to common insulin resistance in type 2 diabetes. Mitochondrial diseases frequently lead to diabetes, which is mostly attributed to defective beta-cell mitochondria and secretion. RESEARCH DESIGN AND METHODS - We assessed muscular mitochondrial function and lipid deposition in liver (hepatocellular lipids [HCLs]) and muscle (intramyocellular lipids [IMCLs]) using P-31/H-1 magnetic resonance spectroscopy and insulin sensitivity and endogenous glucose production (EGP) using hyperinsulinemic-euglycemic clamps combined with isotopic tracer dilution in one female patient suffering from MELAS(myopathy,encephalopathy, lactic acidosis, and stroke-like episodes) syndrome and in six control subjects. RESULTS - The MELAS patient showed impaired insulin sensitivity (4.3 vs. 8.6 +/- 0.5 mg . kg(-1) . min(-1)) and suppression of EGP (69 vs. 94 +/- 1%), and her baseline and insulin-stimulated ATP synthesis were reduced (7.3 and 8.9 vs. 10.6 +/- 1.0 and 12.8 +/- 1.3 mu mol . l(-1) . min(-1)) compared with those of the control subjects. HCLs and IMCLs were comparable between the MELAS patient and control subjects. CONCLUSIONS - Impairment of muscle mitochondrial fitness promotes insulin resistance and could thereby contribute to the development of diabetes in some patients with the MELAS syndrome. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; and
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
host publication
Diabetes Care
volume
32
issue
4
pages
677 - 679
publisher
American Diabetes Association
conference name
68th Annual Meeting of the American-Diabetes-Association
conference dates
2008-06-06 - 2008-06-10
external identifiers
  • wos:000264819800030
  • scopus:65349196063
  • pmid:19131470
ISSN
0149-5992
DOI
10.2337/dc08-2078
language
English
LU publication?
yes
id
0899064f-c461-45fd-83f2-52949a195169 (old id 1401097)
date added to LUP
2016-04-01 13:41:09
date last changed
2025-04-04 13:54:27
@inproceedings{0899064f-c461-45fd-83f2-52949a195169,
  abstract     = {{OBJECTIVE - Impaired muscular mitochondrial function is related to common insulin resistance in type 2 diabetes. Mitochondrial diseases frequently lead to diabetes, which is mostly attributed to defective beta-cell mitochondria and secretion. RESEARCH DESIGN AND METHODS - We assessed muscular mitochondrial function and lipid deposition in liver (hepatocellular lipids [HCLs]) and muscle (intramyocellular lipids [IMCLs]) using P-31/H-1 magnetic resonance spectroscopy and insulin sensitivity and endogenous glucose production (EGP) using hyperinsulinemic-euglycemic clamps combined with isotopic tracer dilution in one female patient suffering from MELAS(myopathy,encephalopathy, lactic acidosis, and stroke-like episodes) syndrome and in six control subjects. RESULTS - The MELAS patient showed impaired insulin sensitivity (4.3 vs. 8.6 +/- 0.5 mg . kg(-1) . min(-1)) and suppression of EGP (69 vs. 94 +/- 1%), and her baseline and insulin-stimulated ATP synthesis were reduced (7.3 and 8.9 vs. 10.6 +/- 1.0 and 12.8 +/- 1.3 mu mol . l(-1) . min(-1)) compared with those of the control subjects. HCLs and IMCLs were comparable between the MELAS patient and control subjects. CONCLUSIONS - Impairment of muscle mitochondrial fitness promotes insulin resistance and could thereby contribute to the development of diabetes in some patients with the MELAS syndrome.}},
  author       = {{Szendroedi, Julia and Schmid, Albrecht Ingo and Meyerspeer, Martin and Cervin, Camilla and Kacerovsky, Michaela and Smekal, Gerhard and Graeser-Lang, Sabine and Groop, Leif and Roden, Michael}},
  booktitle    = {{Diabetes Care}},
  issn         = {{0149-5992}},
  language     = {{eng}},
  number       = {{4}},
  pages        = {{677--679}},
  publisher    = {{American Diabetes Association}},
  title        = {{Impaired Mitochondrial Function and Insulin Resistance of Skeletal Muscle in Mitochondrial Diabetes}},
  url          = {{http://dx.doi.org/10.2337/dc08-2078}},
  doi          = {{10.2337/dc08-2078}},
  volume       = {{32}},
  year         = {{2009}},
}