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. Author manuscript; available in PMC: 2017 Dec 26.
Published in final edited form as: Obesity (Silver Spring). 2017 Jun 26;25(8):1410–1420. doi: 10.1002/oby.21900

Figure 3. Deficiency of Ccr2, Cx3cr1 or both did not modulate HFD-induced hyperglycemia and glucose intolerance in male mice.

Figure 3

Fasting blood glucose levels and IPGTT after an overnight fast were measured prior to and after 4, 8, 14 and 23 weeks of HFD in male WT, Ccr2−/−, Cx3cr1−/− and Cx3cr1−/−Ccr2−/− mice (n=11 WT, 11 Ccr2−/−, 9 Cx3cr1−/−, 14 Cx3cr1−/−Ccr2−/−). A and B: Fasting glucose levels were increased and glucose tolerance was impaired in WT mice by HFD. C and D: Fasting glucose levels or glucose tolerance were similarly affected by HFD between groups (two-way ANOVA analysis), although at 8 weeks of HFD, Ccr2−/− mice showed difference in glucose tolerance at a single-time point. Data are mean±SEM. *, P<0.05 vs. male WT mice.