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One-leg inactivity induces a reduction in mitochondrial oxidative capacity, intramyocellular lipid accumulation and reduced insulin signalling upon lipid infusion: a human study with unilateral limb suspension – published online 17/03/2020

Lena Bilet, Esther Phielix, Tineke van de Weijer, Anne Gemmink, Madeleen Bosma, Esther Moonen-Kornips, Johanna A. Jorgensen, Gert Schaart, Dongyan Zhang, Kenneth Meijer, Maria Hopman, Matthijs K. C. Hesselink, D. Margriet Ouwens, Gerald I. Shulman, Vera B. Schrauwen-Hinderling, Patrick Schrauwen

Physical inactivity is suggested to lead to insulin resistance. An imbalance between skeletal muscle fat accumulation and a low mitochondrial oxidative capacity could determine the development of insulin resistance. However, direct evidence for the role of low mitochondrial function in insulin resistance in humans is lacking. In this issue, Bilet et al (https://doi.org/10.1007/s00125-020-05128-1) investigated whether inactivity-mediated lowering of mitochondrial oxidative capacity affects intramyocellular lipid (IMCL) content and skeletal muscle insulin signalling upon lipid infusion in humans. They report that  the lowering of skeletal muscle mitochondrial function by one-legged immobilisation resulted in IMCL accumulation. In addition, the inactivated leg became more prone to lipid-induced insulin resistance via the activation of protein kinase C θ (PKCθ), as compared with the active leg. The authors conclude that these results illustrate the importance of mitochondrial function in the development of insulin resistance in humans and that lipid-induced insulin resistance occurs via the activation of PKCθ. They suggest that these findings stress the importance of physical activity in the prevention of diabetes.

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