Figure 5.

Drp1 KI mice are protected against diet-induced glucose intolerance and insulin resistance

(A) Body weight evolution during the HFD-feeding period of male Drp1 KI and WT mice.

(B–D) Food intake (B), total activity (C), and energy expenditure (EE) (D) were measured during indirect calorimetry tests using a CLAMS.

(E) Intraperitoneal glucose tolerance tests (2 g/kg) on HFD-fed WT and Drp1 KI mice fasted for 12 h.

(F) Intraperitoneal insulin tolerance tests on HFD-fed WT and Drp1 KI mice fasted for 6 h, using 1 U/kg of insulin.

(G) Thermogenic capacity was evaluated by placing WT and Drp1 KI mice at 6°C and measuring body temperature for 4 h.

(H) Non-shivering thermogenesis in HFD-fed WT and Drp1 KI mice kept at regular housing temperature (22°C) was evaluated by measuring baseline and CL316,243 (1 mg/kg)-induced O₂ consumption in anesthetized mice (n = 10 mice per genotype).

(I) Immediately after the experiment in (C), the mice were housed at thermoneutrality (30°C–33°C) for 4 weeks. Then, non-shivering thermogenesis was measured as in (C).

All values are presented as mean ± SEM of n = 14 WT and n = 11 Drp1 KI, unless otherwise stated. ^∗p < 0.05 and ^∗∗p < 0.01 between WT (white bars and white circles) and Drp1 KI mice (gray bars and black squares). Differences between the two groups were analyzed using a Student’s two-tailed t test in (B)–(D) and (I). Linear mixed-effect models were used in (A) and (E)–(H) to assess time × group interaction effects; subsequent comparisons were performed with Tukey’s honest significant difference post hoc test. See also Figure S5.