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. Author manuscript; available in PMC: 2021 Nov 3.
Published in final edited form as: Cell Metab. 2020 Oct 8;32(5):726–735.e5. doi: 10.1016/j.cmet.2020.09.008

Figure 4. Insulin resistant humans have impaired insulin-stimulated glucose disposal and muscle glycogen synthesis but do not manifest alterations in basal or insulin-stimulated muscle mitochondrial substrate preference (VPDH/VCS).

Figure 4.

A. Insulin resistant subjects have impaired insulin-stimulated peripheral glucose uptake (Rd) compared to insulin sensitive subjects (IS: n=6, IR: n=8). B. Insulin resistant subjects have impaired insulin-stimulated muscle glycogen synthesis (IS: n=6, IR: n=8). C. Measurement of citrate synthase flux by in vivo MRS shows impaired muscle mitochondrial oxidation (VCS) in insulin resistant subjects; estimation of absolute glucose and fat oxidation rates using VPDH/VCS as a multiplier for VCS shows a decrease in both (IS: n=6, IR, n=8). Data are represented as mean ± SEM. D. Skeletal muscle VPDH/VCS in the fasting state is not different between insulin sensitive and insulin resistant subjects. Insulin-stimulation during a hyperinsulinemic-euglycemic clamp significantly increases VPDH/VCS to a similar degree in both groups (IS: n=9, IR: n=9).