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Asian Indians Have Enhanced Skeletal Muscle Mitochondrial Capacity to Produce ATP in Association with Severe Insulin-Resistance

Division of Endocrinology, Endocrine Research Unit, Mayo Clinic College of Medicine, Rochester, MN

Objective: Type 2 diabetes has become a global epidemic; and Asian Indians have a higher susceptibility to diabetes than Europeans. We investigated whether Indians had any metabolic differences compared to Northern European (NE) Americans that may render them more susceptible to diabetes.

Research Design and Methods: We studied thirteen diabetic Indians, thirteen non-diabetic Indians, and thirteen non-diabetic NE Americans who were matched for age, body mass index, and sex. The primary comparisons were insulin sensitivity by hyperinsulinemic-euglycemic clamp and skeletal muscle mitochondrial capacity for oxidative phosphorylation (OXPHOS) by measuring mitochondrial DNA copy number (mtDNA), OXPHOS gene transcripts, citrate synthase activity and maximal mitochondrial ATP production rate (MAPR). Other factors that may cause insulin-resistance were also measured.

Results: The glucose infusion rates required to maintain identical glucose levels during the similar insulin infusion rates were substantially lower in diabetic Indians than in the non-diabetic participants (p<0.001); and were lower in non-diabetic Indians than in non-diabetic NE Americans (p<0.002). mtDNA (P<0.02), OXPHOS gene transcripts (P<0.01), citrate synthase and MAPR (P<0.03) were higher in Indians irrespective of their diabetic status. Intramuscular triglyceride, C-reactive protein, IL-6 and TNF- concentrations were higher, whereas, adiponectin concentrations were lower in diabetic Indians.

Conclusion: Despite being more insulin-resistant diabetic Indians had similar muscle OXPHOS capacity as non-diabetic Indians, demonstrating that diabetes per se does not cause mitochondrial dysfunction. Indians irrespective of their diabetic status had higher OXPHOS capacity than NE Americans, although Indians were substantially more insulin-resistant, indicating a dissociation between mitochondrial dysfunction and insulin-resistance.

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