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. 2017 Feb 9;2(3):e91001. doi: 10.1172/jci.insight.91001

Figure 5. Adipocyte Jak2 is required for growth hormone–induced hepatic insulin resistance and lipolysis.

Figure 5

(A) Plasma glucose levels and (B) glucose infusion rate (GIR) during glucose infusion to achieve euglycemia in vehicle-injected (Veh-injected) control (CON, black circles) and JAK2A (white circles) mice and growth hormone–injected (GH-injected) control (black squares) and JAK2A (white squares) cohorts. (C) GIR at euglycemia in vehicle- and GH-injected control and JAK2A mice. (D) Basal and (E) clamped endogenous glucose production (EGP) in vehicle- and GH-injected control and JAK2A mice. (F) Percentage suppression of EGP following insulin infusion in vehicle- and GH-injected control and JAK2A mice. (G) Whole-body glucose uptake in vehicle- and GH-injected control and JAK2A mice. (H) 2-Deoxyglucose (2-DG) uptake in gastrocnemius and (I) epididymal visceral fat in vehicle- and GH-injected control and JAK2A mice. (J) Basal and (K) clamped plasma free fatty acid (FFA) levels in control and JAK2A mice. (L) Percentage suppression of plasma FFA following insulin infusion in control and JAK2A mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 by 2-way ANOVA (A and B) or 1-way ANOVA (C–L). n = 6–8 for both cohorts. Data represent ± SEM.