In This Issue of Diabetes

Edited by Helaine E. Resnick, PhD, MPH

eNOS Drives Glucose Uptake in Adipose Tissue

Data in this issue of Diabetes show that endothelial nitric oxide synthase (eNOS)–derived nitric oxide (NO) is required in adipose tissue for mitochondrial biogenesis in response to exercise. These results add to a growing body of literature showing the importance of eNOS in mitochondrial biogenesis in a variety of tissues that are relevant in diabetes and glucose metabolism. A key feature of the new report by Trevellin et al. (p. 2800) is that the implications of earlier studies, which focused heavily on the role of eNOS in skeletal and cardiac muscle, have now been firmly extended to adipose tissue. In the new experiments, wild-type (WT) and eNOS-/- mice underwent a progressive exercise regimen, and data from these mice were compared with sedentary WT animals. In the WT mice that were exercised, mitochondrial biogenesis was higher than in the sedentary WT and eNOS-/- mice. Expression of peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α), which regulates mitochondrial biogenesis and function, was also higher in the trained WT animals compared with their eNOS-/- counterparts. Further, a link was demonstrated between exercise and both basal and insulin-stimulated glucose uptake in the WT mice but not the eNOS-/- mice. To understand the potential application of these observations in humans, the investigators studied subcutaneous adipose tissue samples from bariatric surgery patients. The experiments showed that NO promoted mitochondrial biogenesis in human adipocytes and also increased both glucose uptake and GLUT4 translocation. These results contribute to an evolution in thinking about the effect of NO in mediating the impact of exercise in adipose tissue, and they also raise important …

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This Article

  1. doi: 10.2337/db14-ti08 Diabetes vol. 63 no. 8 2565-2566
  1. Free via Open Access: OA