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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 4. Deficiency of Ccr2, Cx3cr1 or both did not affect fasting insulin levels, glucose-induced insulin secretion and insulin sensitivity measured by ITT and hyperinsulinemic euglycemic clamp in HFD-fed male mice.

Figure 4

A: Fasting plasma insulin levels were similar between groups (n=7 WT, 6 Ccr2−/−, 6 Cx3cr1−/−, 6 Cx3cr1−/−Ccr2−/−). B: Glucose-induced insulin secretion (2g/kg glucose by intraperitoneal (i.p.) injection) was similar between groups after 13 weeks of HFD. (n=5 WT, 5 Ccr2−/−, 5 Cx3cr1−/−, 5 Cx3cr1−/−Ccr2−/−). C: ITT test showed similar insulin sensitivity between groups (n=11 WT, 9 Ccr2−/−, 9 Cx3cr1−/−, 14 Cx3cr1−/−Ccr2−/−). D: Hyperinsulinic euglycemic clamp was performed in a representative subgroup of mice (n=6 WT, 5 Ccr2−/−, 6 Cx3cr1−/−, 6 Cx3cr1−/−Ccr2−/−). Fasting hepatic glucose production (HGP) and HGP in response to insulin infusion during the clamp were similar between groups. Glucose infusion rate (GIR) required to maintain euglycemia and Rate of Glucose Disposal (Rd) were also not different. Data are mean±SEM. N.S., not significant.