Fig. 4

The scheme illustrates the role of peripheral clocks in the control of muscle glucose metabolism, as determined using tissue-specific Bmal1 knockout models. The liver clock controls glucose output during the fasting/inactive phase, as shown by the finding that liver-specific Bmal1 KO causes hypoglycemia during this phase [42]. The pancreas β cell clock controls insulin secretion, as β cell-specific Bmal1 KO causes hyperglycemia [43–45]. The muscle clock promotes glucose uptake and metabolism at awakening, as skeletal muscle-specific Bmal1 KO causes impaired insulin-dependent glucose uptake and glucose oxidation in skeletal muscle fibers [27]