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. 2022 Sep 2;14(6):1213–1233. doi: 10.1016/j.jcmgh.2022.08.011

Figure 12.

Figure 12

Liver-specific overexpression of ALKBH1 attenuates HFD-induced insulin resistance. (A) Glucose tolerance tests (GTTs) and its area under the curve (AUC), and (B) insulin tolerance tests (ITTs) and its AUC of control and AOE mice under NCD feeding conditions (n = 6). (C) GTT and its AUC, and (D) ITT and its AUC of control and AOE mice under HFD feeding conditions (n = 6). (E) Immunoblots of factors in insulin signaling pathways in primary hepatocytes, which were transfected with or without Alkbh1-flag for 48 hours, followed with 10 nmol/L insulin or vehicle treatment for 15 minutes. (F) Statistical analysis of the relative protein expression in panel E. (A–D and F) Data are presented as the means ± SD. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P < .0001. Akt, thymoma viral proto-oncogene 1; Alkbh1-flag+Ins, hepatocytes transfected with Alkbh1-flag plasmid and treated with insulin; Alkbh1-flag+Veh, hepatocytes transfected with Alkbh1-flag plasmid and treated with vehicle; AOE, ALKBH1 liver-specific overexpression mice; Blank-flag+Ins, hepatocytes transfected with Blank-flag plasmid and treated with insulin; Blank-flag+Veh, hepatocytes transfected with Blank-flag plasmid and treated with vehicle; GFP, control mice with GFP expression; pAkt, phosphorylated Akt; pGSK3β, phosphorylated glycogen synthase kinase 3 beta.