Impaired mitochondrial function and insulin resistance of skeletal muscle in mitochondrial diabetes
| Autor: | Camilla Cervin, Gerhard Smekal, Michael Roden, Sabine Gräser-Lang, Martin Meyerspeer, Albrecht Ingo Schmid, Michaela Kacerovsky, Leif Groop, Julia Szendroedi |
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| Rok vydání: | 2009 |
| Předmět: |
Adult
Blood Glucose medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Glucose-6-Phosphate Mitochondria Liver Type 2 diabetes Mitochondrion MELAS syndrome Glucose Oxidase Insulin resistance Adenosine Triphosphate Heart Rate Reference Values Internal medicine Diabetes mellitus Internal Medicine medicine Diabetes Mellitus MELAS Syndrome Humans Insulin Intramyocellular lipids Myopathy Muscle Skeletal Pathophysiology/Complications Original Research Advanced and Specialized Nursing business.industry medicine.disease Mitochondria Muscle Endocrinology Spirometry Female medicine.symptom Insulin Resistance business Energy Metabolism |
| Zdroj: | Diabetes Care |
| ISSN: | 1935-5548 |
| Popis: | 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 β-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 31P/1H 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 μmol · 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. |
| Databáze: | OpenAIRE |
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