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Similar findings were reported in mice with deletion of mitochondrial transcription factor A (TFAM) in skeletal muscle and adipose tissue, exhibiting generalized defects in mitochondrial function, expected from the crucial role of TFAM in mitochondrial physiology, that was accompanied by increased glucose uptake in skeletal muscle due to increased glucose transporter 1, while deletion in adipose tissue resulted in resistance to diet-induced obesity, IR, and hepatosteatosis [139, 140]
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