[HTML][HTML] Limited OXPHOS capacity in white adipocytes is a hallmark of obesity in laboratory mice irrespective of the glucose tolerance status
T Schöttl, L Kappler, T Fromme, M Klingenspor - Molecular metabolism, 2015 - Elsevier
T Schöttl, L Kappler, T Fromme, M Klingenspor
Molecular metabolism, 2015•ElsevierObjective Several human and rodent obesity studies speculate on a causal link between
altered white adipocyte mitochondria in the obese state and changes in glucose
homeostasis. We here aimed to dissect whether alterations in white adipocyte mitochondrial
respiratory function are a specific phenomenon of obesity or impaired glucose tolerance or
both. Methods Mature white adipocytes were purified from posterior subcutaneous and
intraabdominal epididymal fat of four murine obesity models characterized by either …
altered white adipocyte mitochondria in the obese state and changes in glucose
homeostasis. We here aimed to dissect whether alterations in white adipocyte mitochondrial
respiratory function are a specific phenomenon of obesity or impaired glucose tolerance or
both. Methods Mature white adipocytes were purified from posterior subcutaneous and
intraabdominal epididymal fat of four murine obesity models characterized by either …
Objective
Several human and rodent obesity studies speculate on a causal link between altered white adipocyte mitochondria in the obese state and changes in glucose homeostasis. We here aimed to dissect whether alterations in white adipocyte mitochondrial respiratory function are a specific phenomenon of obesity or impaired glucose tolerance or both.
Methods
Mature white adipocytes were purified from posterior subcutaneous and intraabdominal epididymal fat of four murine obesity models characterized by either impaired or normal oral glucose tolerance. Bioenergetic profiles, including basal, leak, and maximal respiration, were generated using high-resolution respirometry. Cell respiratory control ratios were calculated to evaluate mitochondrial respiratory function.
Results
Maximal respiration capacity and cell respiratory control ratios were diminished in white adipocytes of each of the four murine obesity models, both in the absence and the presence of impaired glucose tolerance. Limitation was more pronounced in adipocytes of intraabdominal versus subcutaneous fat.
Conclusion
Reduced mitochondrial respiratory capacity in white adipocytes is a hallmark of murine obesity irrespective of the glucose tolerance status. Impaired respiratory capacity in white adipocytes solely is not sufficient for the development of systemic glucose intolerance.
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