Conjugated linoleic acid-induced body fat loss and adipose tissue apoptosis.

摘要

Dietary conjugated linoleic acid (CLA) causes a loss of body fat and the induction of apoptosis in adipose tissue of mice. The body fat loss is enhanced in mice raised from weaning on coconut oil (CO) diets compared to soy oil (SO) diets. CLA is metabolized in the same manner as essential fatty acids (EFA) and CLA metabolites may contribute to the body fat loss. CO is devoid of essential fatty acids, which may be the reason for the enhanced CLA sensitivity in CO-fed mice. The first objective of this work was to determine to what degree the lack of dietary EFA contributes to the CO enhancement of CLA-induced body fat loss. Also, we aimed to determine if CLA metabolism is required for the induction of a loss of body fat. The second objective was to confirm that CLA causes an increase in apoptosis in adipose tissue and to determine if adipogenic cell stage influences sensitivity to CLA. Mice were fed CO only during the 2 wk CLA-feeding period, raised on a fat-free (FF) diet, raised on CO and then replenished with EFA, or fed inhibitors to Delta6-desaturase, cylooxygenase, or lipoxygenase. Body fat was determined by whole body dual X-ray densitometry or individual fat pad weights. Mice fed CO during only the 2 wk they received CLA were leaner (P = 0.06) than mice fed CLA and SO. Replenishment of individual EFA to CO-fed mice did not alter the enhanced response to CLA. All CO+CLA-fed mice were leaner (P 0.001) than SO+CLA-fed mice. Therefore, CO appears to increase CLA sensitivity independent of an EFA deficiency. Inhibiting CLA desaturation blocked the CLA-induced body fat loss. CLA metabolites thus contribute to the body fat loss. However, inhibition of cylooxygenase or lipoxygenase did not affect CLA-induced body fat loss. CLA-induced apoptosis of adipose tissue was confirmed by western blotting for active caspase 3. CLA-fed mice had increased ( P 0.05) cleaved caspase 3 compared to control mice. This was not affected by dietary fat type or the inclusion of any inhibitors. 3T3-L1 cells were treated with CLA or linoleic acid and collected at different stages. Only proliferating cells consistently had increased (P 0.05) DNA fragmentation, a marker of apoptosis, in response to CLA supplementation. In conclusion, CLA metabolites contribute to the body fat loss but not the induction of apoptosis. There does not appear to be a direct interaction between CLA and EFA however.