Background: Conjugated linoleic acid (CLA), a C18 fatty acid with conjugated double bonds, has been shown to serve as a powerful anti-obesity agent by several research groups, although the precise mechanism remains elusive. Previous studies showed that CLA induced apoptosis in 3T3-L1 cells and in mice. The aim of this research was to clarify the role of CLA in adipocyte apoptosis in pigs, a relevant model for obesity research.
Results: Our results clearly show that back fat deposition of CLA-fed pigs was significantly lower than that of pigs in the control group. Moreover, some typical apoptotic cells were observed among the adipocytes of CLA-fed pigs. Furthermore, the CLA-fed pigs had reduced expression of the anti-apoptosis factor Bcl-2 and increased expression of the pro-apoptosis factors Bax and P53. Subsequently, increased cytochrome C was released from the mitochondria to the endochylema, and the caspase cascade was activated, resulting in cellular apoptosis. These results are consistent with the effects of Bcl-2 and Bax in regulating CLA-induced adipocyte apoptosis via the mitochondrial signaling pathway. However, the increased expression of tumor necrosis factor (TNF)-α and its receptor TNFR indicate that the effect of CLA might partly be through the death receptor signaling pathway in adipose cells.
Conclusions: Our study has demonstrated that CLA reduces pig body fat deposition, an outcome that is partly meditated by apoptosis of adipose cells, and that both the mitochondrial pathway and the death receptor pathway are involved in this effect.