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

Författare

  • Julia Szendroedi
  • Albrecht Ingo Schmid
  • Martin Meyerspeer
  • Camilla Cervin
  • Michaela Kacerovsky
  • Gerhard Smekal
  • Sabine Graeser-Lang
  • Leif Groop
  • Michael Roden

Summary, in English

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.

Avdelning/ar

Publiceringsår

2009

Språk

Engelska

Sidor

677-679

Publikation/Tidskrift/Serie

Diabetes Care

Volym

32

Issue

4

Dokumenttyp

Konferensbidrag

Förlag

American Diabetes Association

Ämne

  • Endocrinology and Diabetes

Conference name

68th Annual Meeting of the American-Diabetes-Association

Conference date

2008-06-06 - 2008-06-10

Status

Published

Forskningsgrupp

  • Diabetes - Clinical Obesity
  • Genomics, Diabetes and Endocrinology

ISBN/ISSN/Övrigt

  • ISSN: 0149-5992