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. Author manuscript; available in PMC: 2015 Jul 2.
Published in final edited form as: Nature. 2014 Jun 5;510(7503):84–91. doi: 10.1038/nature13478

Figure 3. Mechanism by which selective skeletal muscle insulin resistance contributes to hepatic insulin resistance.

Figure 3

In insulin-sensitive subjects, insulin stimulates glycogen synthesis in both liver and muscle; however, in those with skeletal muscle insulin resistance, insulin fails to promote glycogen synthesis, diverting substrate to de novo lipogenesis. Increased lipid synthesis in patients with muscle insulin resistance thus produces non-alcoholic fatty liver disease (NAFLD), with increased triglyceride and reduced high-density lipoprotein (HDL) export from the liver. However, these defects in muscle insulin signalling can be reversed by a single 45 minute bout of exercise.