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. Author manuscript; available in PMC: 2016 Mar 3.
Published in final edited form as: Cell Metab. 2015 Mar 3;21(3):443–454. doi: 10.1016/j.cmet.2015.02.009

Figure 5. MOTS-c targets skeletal muscle and regulates insulin sensitivity in mice.

Figure 5

(A) Intraperitoneal glucose tolerance test (1g/kg glucose) in male C57BL/6 mice after MOTS-c treatment (5 mg/kg/day; IP) for 7 days (N=7). (B to E) Euglycemic-hyperglycemic clamps on C57BL/6 mice fed a high-fat diet (60% by calories) and treated with MOTS-c (5 mg/kg/day; IP) for 7 days (N=6-8). (B) Glucose infusion rate (GIR), reflecting whole body insulin sensitivity, (C) insulin-stimulated glucose disposal rate (IS-GDR), primarily reflecting skeletal muscle insulin sensitivity, and (D) hepatic glucose production (HGP). (E) Akt activation (assessed by phosphorylation at Ser473) and MOTS-c levels were detected in the insulin-stimulated skeletal muscles obtained at the end of the hyperinsulinemic-euglycemic clamp. (F and G) MOTS-c levels in young (4-month) and aged (32-month) mice (N=3-4) decline in (F) skeletal muscle, and (G) circulation (serum). (H) Insulin-stimulated (60 μU/ml) 2-deoxyglucose uptake into soleus muscles of young (3-month) and middle-aged (12-month) male C57BL/6 mice after MOTS-c treatment (5 mg/kg/day; IP) for 7 days (N=6). (I-K) Differentiated mature rat L6 myotubes that stably over-express MOTS-c (L6-MOTS-c-ST) show (I) accelerated media glucose clearance, (J) enhanced glucose-stimulated glycolytic response, and (K) maximum glycolytic capacity estimated by oligomycin treatment. Data shown as mean ± SEM. Student's t-test. *P<0.05, **P<0.01, ***P<0.001. See also Table S3.