Relationships between mitochondrial function and metabolic flexibility in type 2 diabetes mellitus.

Research output: Contribution to journalArticleAcademicpeer-review

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 languageEnglish
Article number51648
Number of pages7
JournalPLOS ONE
Volume8
Issue number2
DOIs
Publication statusPublished - 13 Feb 2013

Keywords

  • INTRAMYOCELLULAR LIPID-CONTENT
  • FATTY-ACID-METABOLISM
  • INSULIN-RESISTANCE
  • SKELETAL-MUSCLE
  • GLUCOSE-METABOLISM
  • RESPIRATION
  • EXERCISE
  • OBESE
  • ASSOCIATION
  • DYSFUNCTION

Cite this