CCR2 modulates inflammatory and metabolic effects of high-fat feeding
J. Clin. Invest. Stuart P. Weisberg, et al. 116:115 doi:10.1172/JCI24335 [
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Figure 3Insulin sensitivity in obese
Ccr2–/– and obese
Ccr2+/+ mice.
Fasting plasma insulin (
A) and blood glucose concentrations (
B) were measured in lean
Ccr2+/+ (black bars) and
Ccr2–/– (gray bars) mice and mice of both genotypes made obese following 20 weeks of high-fat diet feeding. There were no significant genotype-dependent differences in fasting glucose or insulin concentrations in lean animals. However, fasting glucose and insulin concentrations were lower in obese
Ccr2–/– compared with obese
Ccr2+/+ mice despite similar degrees of adiposity (insulin:
P < 0.005; glucose:
P < 10
–4). (
C) HOMA-IR values (expressed as IU-mg/dl) were significantly lower (
P < 10
–4) among obese
Ccr2–/– than obese
Ccr2+/+ mice. (
D) A plot of HOMA-IR values against body mass among all
Ccr2–/– (gray squares) and
Ccr2+/+ (black circles) mice reveals that the relationship between insulin sensitivity and body mass differs between mice dependent upon
Ccr2 genotype. **
P < 0.01 compared with wild type. Values are expressed as mean ± SD.