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Differential expression of Pparγ target genes in testis of rats under theinfluence of paternal trans fatty acid and vitamin-E

Cell J. 2026 Feb 28;27(1):1-13. doi: 10.22074/cellj.2026.2050175.1770.

ABSTRACT

OBJECTIVE: A paternal high-fat diet (HFD) has been shown to affect the expression of peroxisome proliferator-activated receptors (Ppars), particularly in offspring’s testicle regions. One of its isoforms, Pparγ, participates in spermatogenesis as a transcription factor regulating fatty acid metabolism genes. This study aimed to investigate how paternal dietary intake of trans fatty acids and/or vitamin E influences the expression of Pparγ target genes in the testes of their offspring, with the goal of elucidating potential mechanisms related to altered lipid metabolism and reproductive health.

MATERIALS AND METHODS: In this experimental study, adult male Wistar rats (F0) were fed for 60 days with one of the following four diets: control diets (C), control diets with trans fatty acids (CTH), diets containing vitamin E (E) and diets containing vitamin E and trans fatty acids (ETH). Then the male offspring (F1) were raised on standard chow, and their testicular tissue was later analyzed to assess the impact of paternal diet on gene expression, and the expression of the Pparγ target genes: Elovl2, Muc1, Fads2, Scd1, Glut2 and Lpl were measured quantitatively.

RESULTS: The data revealed that paternal HFD can suppress the expression of Pparγ target genes in the testes of offspring. Fads2, Elovl2 were significantly upregulated in response to paternal vitamin E supplementation. The changes in Lpl gene expression were not statistically significant. Also, co-expression analysis and functional enrichment approach indicated that the genes involved in cellular response to fatty acid, fatty acid metabolic process, lipid storage, and fatty acid biosynthetic process were overexpressed in up/down regulated Pparγ target genes.

CONCLUSION: Our findings demonstrate the metabolic impact of paternal diet on offspring’s, with focus on mechanisms related to altered lipid metabolism and reproductive health.

PMID:42001274 | DOI:10.22074/cellj.2026.2050175.1770

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