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. 2011 Jun 20;60(7):1861–1871. doi: 10.2337/db11-0030

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© 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 5. — FXR deficiency protects from diet-induced obesity and insulin resistance. FXR^+/+ (white bars or circles) and FXR^−/− mice (black bars or circles) (n = 7–11/group) were fed a HFD for 20 weeks. A: Body weight was monitored weekly (n = 7–11/group). Significance of the overall effect of genotype (P < 0.0001) and age (P < 0.0001) as well as their interaction (P < 0.0001) was calculated by two-way ANOVA. Plasma leptin (B), plasma triglyceride (TG) (C), blood glucose (D), and plasma insulin (E) were determined at the end of the feeding period (n = 4–9/group). Blood glucose excursion (F) and integrated AUC (G) after administration of an intraperitoneal glucose bolus (1 g/kg glucose) were measured at the end of the feeding period (n = 6–9/group). Significance of the overall effect of genotype (P < 0.0001) and time (P < 0.0001) was calculated by two-way ANOVA. Values are means ± SEM. Differences between genotypes over time were analyzed by two-way ANOVA and Bonferroni post hoc test; differences between genotypes were calculated by Mann-Whitney test (*P < 0.05, **P < 0.01, ***P < 0.001).