Figure 4. aP2-Prdm16 mice are protected from obesity and metabolic dysfunction upon high-fat feeding.
(A) Body weights of WT and aP2-Prdm16 mice during 10-week time course of high-fat feeding. (B) MRI was used to analyze body composition (fat and lean mass) in WT and aP2-Prdm16 mice after 16 weeks of high-fat diet. (C) Energy expenditure and food intake was measured for 72 hours in individually housed WT and aP2-Prdm16 mice after 1 week of high-fat diet. Energy expenditure is reported as VO2/mouse/hour. (D) Glucose tolerance test. Blood glucose levels were measured in 16-week high-fat diet–fed WT or aP2-Prdm16 mice after an overnight fast (time 0) and at the indicated times after intraperitoneal injection of glucose. (E) Insulin tolerance test. Blood glucose levels were measured after an overnight fast (time 0) and at the indicated times after an intraperitoneal injection of insulin in mice from D. (F) Immunohistochemistry for Ucp1 (brown stain) protein in ingWAT from WT and aP2-Prdm16 mice after 16 weeks of high-fat diet. The boxed region is shown at higher magnification at right. Ucp1-expressing multilocular and unilocular fat cells are indicated by the arrow and arrowhead, respectively. Original magnification, ×20 (left and middle); ×100 (right). mRNA levels of brown fat–selective genes (Ucp1 and Cidea) were determined in epidWAT, ingWAT, and iBAT from WT and aP2-Prdm16 animals after 16 weeks of high-fat diet. Significance between curves was determined by 2-way ANOVA. Values are mean ± SEM (n = 16 mice per group per experiment). *P < 0.05, **P < 0.01 vs. WT.