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

Abstract

Objectives were to determine adipose tissue mRNA expression of peroxisome proliferator-activated receptor (PPAR)γ 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, β-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 SFAT 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 PPARγ. 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 PPARγ-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.

Effects of fish oil and additional starch on tissue fatty acid profile and lipogenic gene mRNA abundance in lactating goats fed a diet containing sunflower-seed oil

“…In the present study, PPARG1 mRNA abundance was high in the omental and perirenal ATs, with no differences between them, whereas SREBF1 mRNA abundance, which could be involved in the anabolic pathways related to PPARG signalling in AT (Schmitt et al, 2011), was higher in the perirenal than in the omental site. Relatively high mRNA abundances of LXRA were found in both ATs; further, in the omental site, LXRA was also strongly correlated with CD36 and PPARA transcripts (r 5 0.96, P , 0.001; and r 5 0.91, P 5 0.002, respectively), which suggests a similar regulation for each pair of genes.…”

“…Among the transcription factors that have been characterised in ruminants, PPARG1 seems to be the major regulator of lipid metabolism in AT (Sundvold et al, 1997;Schmitt et al, 2011). In the present study, PPARG1 mRNA abundance was high in the omental and perirenal ATs, with no differences between them, whereas SREBF1 mRNA abundance, which could be involved in the anabolic pathways related to PPARG signalling in AT (Schmitt et al, 2011), was higher in the perirenal than in the omental site.…”

Dietary sunflower oil modulates milk fatty acid composition without major changes in adipose and mammary tissue fatty acid profile or related gene mRNA abundance in sheep

“…Studies on diet-induced MFD in cows report an increase in the mRNA abundance of lipogenic genes in AT related to the preferential partitioning of nutrients towards non-mammary tissues (Harvatine et al, 2009;Thering et al, 2009;Schmitt et al, 2011). On the contrary, lipid supplementation inducing no changes or increases in milk fat yield in goats is not accompanied by alterations of the mRNA abundance or activity of lipogenic enzymes in AT (Bernard et al, 2005a and2009a).…”

O-GlcNAcylation of co-activator-associated arginine methyltransferase 1 regulates its protein substrate specificity

“…CARM1 was shown to be a co-activator of PPARγ [5], a key transcription factor regulating glucose and lipid metabolism. The expression level of CARM1 in cattle liver [66] and subcutaneous adipose tissue [67] is sensitive to types of fatty acid in diet. Moreover, CARM1 regulates expression of key enzymes in gluconeogenesis [68] and glycogen metabolism [69].…”

“…A few studies have implicated CARM1 as a regulator of cellular metabolism [5,[66][67][68][69]. CARM1 was shown to be a co-activator of PPARγ [5], a key transcription factor regulating glucose and lipid metabolism.…”