Short communication: Effect of trans-10,cis-12 conjugated linoleic acid on activation of lipogenic transcription factors in bovine mammary epithelial cells

Abstract The objective of this study was to examine the effect of trans -10, cis -12 conjugated linoleic acid ( t 10 c 12CLA) on the activation of transcription factors that potentially regulate lipid synthesis in a bovine mammary epithelial cell line (MAC-T). Cells were transfected with luciferase reporter constructs containing sterol response element (SRE and SRE complex) for sterol regulatory element binding protein-1, peroxisome proliferator response element for peroxisome proliferator-activated receptor γ, or liver X receptor response element for liver X receptor. Different concentrations of t 10 c 12CLA (0, 25, 50, 75, or 100μ M ) were applied to cells to determine the activation of transcription factors. The influence of t 10 c 12CLA bond structure on transcription factor activation was also investigated by treating cells with different 18:1 fatty acid isomers ( trans- 10 18:1 or cis- 12 18:1) at 100μ M . Cells were harvested for luciferase assay after 24h of treatment. Compared with linoleic acid and cis -9, trans -11 CLA controls, the SRE reporters had significantly lower activity in t 10 c 12CLA-treated cells at 50 and 75μ M for SRE complex and SRE, respectively. Lower SRE and SRE complex activation was observed in t 10 c 12CLA treatment at 25, 50, and 75μ M compared with 0μ M . The peroxisome proliferator response element and liver X receptor response element reporters did not respond differently between the t 10 c 12CLA treatment and controls. Compared with t 10 c 12CLA, both trans- 10 18:1 and cis- 12 18:1 increased the activities of SRE and SRE complex reporters by 1.3- to 4.2-fold. In conclusion, t 10 c 12CLA has an inhibitory role in lipogenic transcription factor activation of SRE, and this negative effect is due to the conjugation of trans- 10 and cis- 12 double bonds in the fatty acid. Furthermore, we found no support for a regulatory role of response elements for peroxisome proliferator-activated receptor γ or liver X receptor in the t 10 c 12CLA inhibition of mammary lipid synthesis.