Endocrine Abstracts

Introduction: Deranged mitochondrial biogenesis has been linked to obesity with or without type 2 diabetes but this association has not been reported in non obese type 2 diabetes subjects. This study attempts to identify the various alterations of mitochondrial biogenesis in adipose tissue in obese and non obese type 2 diabetes subjects.

Methods & Design: Since type 2 diabetes is associated with elevated serum leptin and depressed serum adiponectin levels, these parameters were measured in four different groups of subjects- non obese non diabetic (C), non diabetic obese (OB), non obese type 2 diabetes (NOT2D) and obese type 2 diabetes (T2D+OB). Mitochondrial biogenesis was assessed in subcutaneous adipose tissue by estimating the content of several mitochondrial proteins e.g. cytochrome c, ND4L (subunit of complex I), COX 2 (subunit of complex IV etc.) and transcription factors in whole adipose tissue lysate and isolated mitochondria. A cell based model has been designed to examine the role of mitochondria in adipokine secretion and synthesis.

Results: There was a linear increase in serum leptin levels and decrease in serum adiponectin levels from OB to T2D+OB but remained unchanged in NOT2D compared to C. Mitochondrial biogenesis was significantly impaired in adipose tissue of OB and more remarkably in T2D+OB but remains unaffected in NOT2D. This aspect is being investigated in our cell based model.

Conclusion: High serum leptin levels and hypoadiponectinemia were not observed in NOT2D patients. This may account for the relative ineffectiveness of insulin sensitizers in NOT2D subjects as reported previously. Similarly, the absence of impaired mitochondrial biogenesis in NOT2D is an important finding which indicates the critical importance of obesity in mitochondrial pathology of type 2 diabetes. Other pathogenic aspects need to be explored in NOT2D subjects.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.