Comment on De Wendt et al. Contraction-Mediated Glucose Transport in Skeletal Muscle Is Regulated by a Framework of AMPK, TBC1D1/4, and Rac1. Diabetes 2021;70:2796–2809

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In their study, de Wendt et al. (1) present evidence to suggest that the full effect of contraction on muscle glucose uptake is regulated by a framework of proteins consisting of AMPK, TBC1D1, TBC1D4, and Rac1. Their work is based on experiments performed in isolated and incubated skeletal muscle from a novel mouse model deficient in muscle AMPK combined with whole-body knockout of TBC1D1 and TBC1D4. From a mechanistic point of view, the experimental ex vivo mouse muscle model used is strong, as it permits accurate assessment of glucose uptake in isolated muscle during contraction in the absence of confounding factors that may persist in the intact animal model (2).
In their study, de Wendt et al. (1) present evidence to suggest that the full effect of contraction on muscle glucose uptake is regulated by a framework of proteins consisting of AMPK, TBC1D1, TBC1D4, and Rac1. Their work is based on experiments performed in isolated and incubated skeletal muscle from a novel mouse model deficient in muscle AMPK combined with whole-body knockout of TBC1D1 and TBC1D4. From a mechanistic point of view, the experimental ex vivo mouse muscle model used is strong, as it permits accurate assessment of glucose uptake in isolated muscle during contraction in the absence of confounding factors that may persist in the intact animal model (2).
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