Abstract
Introduction: Mitochondrial dysfunction, lipid accumulation, insulin resistance and metabolic inflexibility have been implicated in the etiology of type 2 diabetes (T2D), yet their interrelationship remains speculative. We investigated these interrelationships in a group of T2D and obese normoglycemic control subjects.
Methods: 49 non-insulin dependent male T2D patients and 54 male control subjects were enrolled, and a hyperinsulinemic-euglycemic clamp and indirect calorimetry were performed. A muscle biopsy was taken and intramyocellular lipid (IMCL) was measured. In vivo mitochondrial function was measured by PCr recovery in 30 T2D patients and 31 control subjects.
Results: Fasting NEFA levels were significantly elevated in T2D patients compared with controls, but IMCL was not different. Mitochondrial function in T2D patients was compromised by 12.5% (p
Conclusions: These results indicate that defects in skeletal muscle in vivo mitochondrial function in type 2 diabetic patients are only reflected in basal substrate oxidation and highlight the importance of glucose disposal rate as a determinant of substrate utilization in response to insulin.
Original language | English |
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Article number | 51648 |
Number of pages | 7 |
Journal | PLOS ONE |
Volume | 8 |
Issue number | 2 |
DOIs | |
Publication status | Published - 13 Feb 2013 |
Keywords
- INTRAMYOCELLULAR LIPID-CONTENT
- FATTY-ACID-METABOLISM
- INSULIN-RESISTANCE
- SKELETAL-MUSCLE
- GLUCOSE-METABOLISM
- RESPIRATION
- EXERCISE
- OBESE
- ASSOCIATION
- DYSFUNCTION