# Potential involvement of peroxisome proliferator-activated receptors in the inhibition of mammary lipid synthesis during diet-induced milk fat depression

## TL;DR

This study investigates whether peroxisome proliferator-activated receptors (PPARs) are involved in milk fat depression in dairy cows caused by diet or CLA.

## Contribution

The study provides evidence that PPARs do not play a functional role in milk fat depression in dairy cows.

## Key findings

- PPAR-α and PPAR-β/δ have low expression in mammary tissue compared to the liver.
- PPAR isoform expression increases during lactation but remains largely unchanged during milk fat depression.
- PPAR-γ activation does not counteract CLA-induced inhibition of milk fat synthesis.

## Abstract

The objective of this study was to evaluate the possible role of the peroxisome proliferator-activated receptors (PPAR: PPAR-α, PPAR-β/δ, and PPAR-γ) in diet and CLA-induced milk fat depression (MFD) in dairy cows. We hypothesized that the expression of PPAR, which regulate lipid metabolism and bind to PUFA, could be modulated by biohydrogenation intermediates that induce MFD, thereby interfering with milk fat synthesis. First, tissue profiling revealed that PPAR-α and PPAR-β/δ had low expression in mammary tissue compared with the liver. A comparison of lactating and nonlactating tissue from the same cows showed that expression of all 3 PPAR isoforms did increase during lactation. Mammary expression of the PPAR family during MFD was then observed in 9 mid-lactation cows in a 3 × 3 Latin square design with MFD induced by a 3-d intravenous infusion of trans-10,cis-12 CLA or feeding a high-oil and low-forage diet. The expression of all 3 PPAR isoforms remained largely unaltered during CLA and diet-induced MFD, except for an increase in PPAR-α target genes CPT1A and ACADVL that are involved in β-oxidation. The interaction of PPAR-γ chemical agonist troglitazone and antagonist T0070907 and CLA was then investigated in bovine mammary epithelial cells. The activation and inhibition of PPAR-γ did not overcome trans-10,cis-12 CLA inhibition of lipogenesis despite the agonist stimulating PPAR-γ expression. Furthermore, PPAR-γ activation did not modify the expression of lipogenic genes. Overall, the results fail to support a functional role of the PPAR family in the inhibition of lipogenesis during MFD in dairy cows.