ArticleScientific reports2021
Fatty acids suppress the steroidogenesis of the MA-10 mouse Leydig cell line by downregulating CYP11A1 and inhibiting late-stage autophagy.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026Review
- Microsomal triglyceride transfer protein restricts steroid production in Leydig cells by regulating SREBP2.iScience · 2026Article
- The hemopexin domain of matrix metalloproteinase-9 attenuates lipopolysaccharide-induced interleukin-6 secretion in liver.Scientific reports · 2025Article
- Mechanisms of Leydig Cell Aging and Obesity-Related Hypogonadism in Men: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Molecular characterization of the murine Leydig cell lines TM3 and MLTC-1.Frontiers in endocrinology · 2025Article
- Functional role of autophagy in testicular and ovarian steroidogenesis.Frontiers in cell and developmental biology · 2024Review
- The constructive and destructive impact of autophagy on both genders' reproducibility, a comprehensive review.Autophagy · 2023Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
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Abstract
Obese men have lower circulating testosterone than men with an optimal body mass index. Elevated fatty acids (FAs) caused by obesity have been reported to suppress the steroidogenesis of Leydig cells. Recent studies have demonstrated that autophagy regulates steroidogenesis in endocrine cells; however, few studies have investigated the molecular mechanisms of FA-impaired steroidogenesis. To study FA regulation in the steroidogenesis of Leydig cells, MA-10 cells were treated with an FA mixture and co-treated with 8-Br-cAMP to stimulate the steroidogenesis capacity. We showed that FAs led to cellular lipid accumulation and decreased steroidogenesis of MA-10 cells, and FA-suppressed steroidogenesis was largely recovered by P5 treatment but not by 22R-OHC treatment, suggesting the primary defect was the deficiency of CYP11A1. To examine the involvement of autophagy in the steroidogenesis of Leydig cells, we treated MA-10 cells with autophagy regulators, including rapamycin, bafilomycin, and chloroquine. Inhibition of late-stage autophagy including FA-upregulated Rubicon suppressed the steroidogenesis of MA-10 cells. More interestingly, Rubicon played a novel regulatory role in the steroidogenesis of MA-10 cells, independent of inhibitors of late-stage autophagy. Collectively, this study provides novel targets to investigate the interaction between FAs and steroidogenesis in steroidogenic cells.
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