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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Nat Med. 2015 Mar 23;21(4):373–382. doi: 10.1038/nm.3826

Figure 6.

Figure 6

MKP1 reduction is required for nicotine-mediated IR and lipolysis. (a–g) WT and Mkp1−/− mice were treated with Veh or Nic. (a) Body weight changes and fat mass in mice treated with Veh or Nic; n = 7–8 each. (b) In vivo lipolysis. Plasma glycerol concentration measured at 0, 15, 60, 120 min; n = 6 each. (c,d) IPGTT (c) and ITT (d) data in mice; n = 7–8 each. (e,f) The glucose infusion rate (GIR) (e) and the hepatic glucose production (HGP), the rate of the disappearance (Rd) and in tibialis anterior and soleus muscles or eWAT the glucose metabolic index (Rg) (f) during a hyperinsulinemic-euglycemic clamp (n = 6 each). (g) MKP1, pIrs1- Ser307, Irs1 and p38 signaling in WAT of mice of the indicated genotype; n = 6 each. (h) AchRα7 expression in isolated adipocytes, hepatocytes, β-cells, and myocytes after treatment with Nic or Veh; n = 6 each. (i) Detection of pAMPK, AMPK, MKP1, and Irs1 expression in WAT in smokers and nonsmokers; n = 12 each. (j) Oral glucose tolerance test (OGTT) (left), the insulin levels during OGTT (right) and the areas under the curve (AUC); n = 12 each. Significance determined by one-way ANOVA with Bonferroni’s post-hoc test (a,f,g,j), one-way ANOVA with repeated measures for the inter-assay evaluations (b,c,d,e), Student’s t-test (h,i), *P < 0.05 Veh vs.Nic, and #P < 0.05 WT vs. Mkp1−/− mice. All values are means ± SEM.