Fig. 1. Body weights for control and CLA treated mice fed high-fat or low-fat diets for 6 weeks. CLA significantly reduced body weight gain in the high-fat (*) and low-fat () diet groups (p<0.001).
Fig. 2. Adipose depot weights for mice control and CLA treated mice fed high- or low-fat diets. CLA treatment significantly reduced adipose depot weights in the high-fat (*) and low-fat () diet groups (p<0.001).
Fig. 3. Energy expenditure after 6 weeks of CLA treatment for mice fed a high-fat or a low-fat diet. CLA treatment significantly increased energy expenditure in the high-fat (*) and low-fat () diet groups (p<0.01).
Fig. 4. Respiratory quotient after 6 weeks of CLA treatment in mice fed a high-fat or low-fat diet. CLA treatment blocked the increased RQ observed during the feeding period (night), indicating increased fat oxidation.
Fig. 5. Adipose depot weights in mice fed increasing doses of CLA in a high-fat diet. *Cumulative adipose depot weight was reduced with 0.5% CLA (p<0.01). The retroperitoneal depot was the most responsive to CLA treatment.
Fig. 6. Body weights of control and 1% CLA treatment over 12 weeks. *CLA treatment significantly reduced body weight by 4 weeks of treatment (p<0.001)..
Fig. 7. Adipose depot weights for control and CLA treated mice fed a high-fat diet. *Cumulative adipose depot weight was reduced after 4 weeks of CLA treatment (p<0.001). The retroperitoneal depot was reduced after 2 weeks (p<0.001), the inguinal and epididymal after 4 weeks (p<0.05), and the mesenteric after 6 weeks (p<0.001) of CLA treatment.
Fig. 8. Energy expenditure of control and 1% CLA treated mice over 5 weeks. Overall, CLA treatment significantly increased daytime and nighttime energy expenditure (p<0.05).
) diet groups (p<0.001).
