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. Author manuscript; available in PMC: 2012 Apr 11.
Published in final edited form as: Science. 2012 Mar 30;335(6076):1638–1643. doi: 10.1126/science.1215135

Figure 1.

Figure 1

Rapamycin-induced insulin resistance is independent of hepatic mTORC1. A-F) Glucose infusion rate (A), rate of disappearance of glucose from the circulation (B), hepatic gluconeogenesis (C) and insulin responsiveness (D), as well as glucose uptake by white adipose tissue (E) and skeletal muscle (F) were determined during a hyperinsulinemic-euglycemic clamp in mice treated with 2 mg/kg/day rapamycin or vehicle control for two weeks. (Each dot represents a single animal, n = 13 vehicle-treated mice, 11 rapamycin-treated mice, * = P < 1×10-5, Student’s t-test; # = P < 0.045 by Brown-Mood k-sample median test.) G) Serum glucose and insulin concentration in rapamycin-treated mice during fasting and after re-feeding for 4 hours (* = P < 0.02). H) Phosphorylation of the mTORC1 substrate S6K1 T389 and subsequent phosphorylation of S6 in the livers of rapamycin-treated mice. I,J) Glucose tolerance with or without rapamycin treatment in mice lacking hepatic Raptor (* = P < 0.05, # = P < 0.06 for rapamycin treated groups vs. untreated). All bars indicate mean and SEM.