Introduction: Deranged Mitochondrial bioenergetics is a key feature of type 2 diabetes and obesity but its status in non-obese type 2 diabetes patients is not known. The aim of the present study was to assess the status of mitochondrial oxidative phosphorylation and ROS metabolism in subcutaneous adipose tissue isolated from 4 groups of subjects: non-obese subjects with type 2 diabetes (NOT2D), non-obese non diabetic (C), obese non-diabetic (OB) and obese type 2 diabetes subjects (OB+T2D).
Methods & Design: Mitochondria were isolated from subcutaneous white adipose tissue of four groups of subjects under study: C, NOT2D, OB, and OB+T2D. The activities of respiratory complexes, the trans-membrane potential and the phosphate utilization capacity of adipose tissue mitochondria from these groups were measured. The rate of ROS (reactive oxygen species) formation, the levels of protein and lipid oxidation markers and the activities of SOD and catalase were also measured.
Results: There was a progressive decrease in mitochondrial transmembrane potential, phosphorylation capacity and the activities of respiratory chain complexes from OB to OB+T2D, whereas such parameters remained unaffected in NOT2D, compared to C. However, markers of oxidative stress and damage increased in adipose tissue mitochondria in a progressive manner from NOT2D to OB+T2D.
Conclusion: Mitochondrial bioenergetics was unaffected in NOT2D subjects, whereas a linear increase in ROS production and metabolism were observed from NOT2D to OB+T2D. Therefore, alteration in mitochondrial bioenergetics cannot fully explain the ROS production in all three groups. This raises the possibility of existence of some extra-mitochondrial pathway accounting for increased ROS production in the affected subjects. Our results may also possibly be explained by altered anti-oxidant enzyme status in the patient population under study.
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.
05 - 09 May 2012
European Society of Endocrinology