Dietary lipid during the transition period to manipulate subcutaneous adipose tissue peroxisome proliferator-activated receptor-γ co-regulator and target gene expression

Objectives were to determine adipose tissue mRNA expression of peroxisome proliferator-activated receptor (PPAR)gamma co-regulators; target enzymes and transcription regulators, inflammation-related genes, and adipokines in response to dietary long-chain fatty acids (LCFA). From -21 through 10 d relative to parturition cows were fed no supplemental LCFA (control), saturated LCFA (SFAT; mainly 16:0 and 18:0), or fish oil (FO). Lipid was fed at 250 g/d prepartum or approximately 1.5 to 1.9% of the previous day's dry matter intake postpartum. Transcript profiling of 35 genes via quantitative PCR was conducted on biopsies (n = 5 cows/diet) collected at 14 and 11 d from parturition. Despite lower dry matter intake with FO, pre- and postpartal blood nonesterified fatty acids, beta-hydroxybutyrate and liver triacylglycerol were unaffected by treatment but increased after calving regardless of diet. Prepartal expression of adipogenic/lipogenic transcription regulators [CEBPA, CEBPB, RXRA, KLF5, and MLXIPL (formerly ChREBP)] and co-regulators (CARM1, EP300, NCOA1, MED1, NCOR2, and NRIP1) was upregulated by FO and SFAT versus control, whereas most enzymes involved in lipogenesis/triacylglycerol synthesis (FASN, SCD, DGAT2, and LPIN1) had greater expression only with FO. Expression of most adipogenic/lipogenic genes decreased after parturition, but feeding SEAT led to sustained upregulation of CEBPA, CEBPB, RXRA, several PPAR-co-activators, and DGAT2 and SCD, suggesting maintenance of a pro-adipogenic/pro-lipogenic state with SFAT. The co-activator CREBBP was greater in cows fed lipid and did not decrease after parturition, suggesting ligand activation of PPAR gamma. The greater peripartal expression of NFKB1 and TBK1 due to dietary lipid was suggestive of a local inflammatory response. At amounts fed prepartum, both FO and SFAT were effective in upregulating the adipose tissue PPAR gamma-gene network. In contrast, only SFAT led to sustaining that response. Overall, the observed expression patterns are suggestive of an adipogenic regulatory mechanism particularly responsive to SFAT.