ArticleJournal of dairy science2025
Potential involvement of peroxisome proliferator-activated receptors in the inhibition of mammary lipid synthesis during diet-induced milk fat depression.
Article in Journal of dairy science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Genome-Wide Association Study Revealed Key Genes with the Teat Number in Jishen Black Pigs.Veterinary sciences · 2026Article
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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.
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Registered trials
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