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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 1. HFD feeding induces muscle insulin resistance and defects in insulin signaling but these changes are not associated with alterations in muscle mitochondrial substrate preference.

Figure 1.

A-B. HFD-fed rats have normal fasting blood glucose but higher plasma insulin levels. C. Muscle of insulin-resistant rats exhibit impaired IRK tyrosine1162 phosphorylation. D. Muscle of insulin-resistant rats exhibit impaired IRS-1-associated PI3K activity. E. Muscle of insulin-resistant rats has impaired insulin signaling as measured by AKT serine473 phosphorylation. F. HFD-fed rats have impaired muscle glucose uptake as measured by peripheral glucose disposal (Rd). G. HFD-fed rats have impaired muscle glucose transport as measured by 2-[14C]deoxyglucose (2-DG) uptake. H-I. HFD-fed insulin resistant rats do not exhibit altered VPDH/VCS fluxes in soleus and quad muscles in the fasting state. Insulin stimulation during a clamp increases VPDH/VCS in muscle in both groups, but is blunted in HFD-fed rats. 2-DG uptake measured in soleus, other muscle measures in quadriceps muscle due to limitation in the amount of tissue. Data are represented as mean ± SEM.