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Mitochondrial bioenergetics is not impaired in nonobese subjects with type 2 diabetes mellitus
Authors:Chattopadhyay Mrittika  Guhathakurta Ishita  Behera Prajna  Ranjan Kumar Rajeev  Khanna Manoj  Mukhopadhyay Satinath  Chakrabarti Sasanka
Affiliation:aDepartment of Biochemistry, Institute of Post Graduate Medical Education & Research, Kolkata-700020, India;bDepartment of Surgery, Institute of Post Graduate Medical Education & Research, Kolkata-700020, India;cCosmetic Surgery Clinic, Kolkata-700017, India;dDepartment of Endocrinology and Metabolism, Institute of Post Graduate Medical Education & Research, Kolkata-700020, India
Abstract:Although mitochondrial dysfunction has been well documented in obese people with type 2 diabetes mellitus, its presence or absence in nonobese subjects with type 2 diabetes mellitus has not been well studied so far. The aim of the present study was to assess the status of mitochondrial oxidative phosphorylation in subcutaneous adipose tissue of nonobese type 2 diabetes mellitus subjects in comparison to control, obese nondiabetic, and obese type 2 diabetes mellitus subjects. Mitochondria were isolated from subcutaneous white adipose tissue obtained from the abdominal region of control, obese nondiabetic, nonobese type 2 diabetes mellitus, and obese type 2 diabetes mellitus subjects. The activities of complex I, I to III, II to III, and IV; transmembrane potential; and inorganic phosphate utilization of mitochondria from different groups were measured. Mitochondrial transmembrane potential, inorganic phosphate utilization, and the activities of respiratory chain complexes were significantly reduced in obese nondiabetic and obese type 2 diabetes mellitus patients compared with those in control subjects. No detectable change in mitochondrial functional parameters was observed in case of nonobese type 2 diabetes mellitus subjects compared with control subjects. Furthermore, a significant difference was noticed in mitochondrial phosphate utilization and activities of respiratory complexes, for example, I, I to III, and II to III, between obese type 2 diabetes mellitus subjects and obese nondiabetic subjects. Obesity modulates mitochondrial dysfunction associated with type 2 diabetes mellitus.
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