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<p>Polycystic ovary syndrome (PCOS) is characterized by insulin resistance and metabolic dysfunction. Mitochondrial-derived peptides (MDPs), including MOTS-c, regulate glucose homeostasis and skeletal muscle metabolism. Whether MOTS-c expression is altered in PCOS across different physiological compartments remains unknown. The aim was to assess circulating and skeletal muscle MOTS-c levels in women with PCOS and to examine their associations with metabolic and hormonal parameters. Forty women with PCOS and 40 age- and BMI-matched healthy controls underwent clinical, biochemical, and hormonal phenotyping. Serum MOTS-c concentrations were quantified by ELISA. In a representative subgroup, skeletal muscle MOTS-c expression was assessed in vastus lateralis biopsy specimens using Western blotting. Women with PCOS exhibited lower circulating MOTS-c concentrations compared with controls (220.2 ± 147.6 pg/mL vs. 498.3 ± 224.4 pg/mL, <i>p</i> &lt; 0.001). Skeletal muscle MOTS-c expression was also reduced in the PCOS group (74.2 ± 15.2 vs. 100.0 ± 8.5 arbitrary units; <i>p</i> = 0.005). Serum MOTS-c levels were inversely associated with total testosterone (<i>r</i> = − 0.224, <i>p</i> = 0.046) and total cholesterol (<i>r</i> = − 0.228, <i>p</i> = 0.044). Women with PCOS display reduced MOTS-c expression in both the circulation and skeletal muscle, suggesting reduced availability of this mitochondrial-derived peptide. Associations with hyperandrogenism and lipid profiles suggest a potential link between altered mitochondrial peptide biology and the endocrine–metabolic phenotype of PCOS. These findings suggest that MOTS-c may represent a potential marker of tissue-specific mitochondrial involvement in PCOS and warrant further investigation.</p>

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Reduced serum and skeletal muscle MOTS c levels in women with polycystic ovary syndrome are associated with mitochondrial dysfunction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月12日

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  • Irem Sonmezoglu Kutuk,
  • Senay Akin,
  • Haydar Demirel,
  • Sezcan Mumusoglu,
  • Turkmen Ciftci,
  • Bulent Okan Yildiz

摘要

Polycystic ovary syndrome (PCOS) is characterized by insulin resistance and metabolic dysfunction. Mitochondrial-derived peptides (MDPs), including MOTS-c, regulate glucose homeostasis and skeletal muscle metabolism. Whether MOTS-c expression is altered in PCOS across different physiological compartments remains unknown. The aim was to assess circulating and skeletal muscle MOTS-c levels in women with PCOS and to examine their associations with metabolic and hormonal parameters. Forty women with PCOS and 40 age- and BMI-matched healthy controls underwent clinical, biochemical, and hormonal phenotyping. Serum MOTS-c concentrations were quantified by ELISA. In a representative subgroup, skeletal muscle MOTS-c expression was assessed in vastus lateralis biopsy specimens using Western blotting. Women with PCOS exhibited lower circulating MOTS-c concentrations compared with controls (220.2 ± 147.6 pg/mL vs. 498.3 ± 224.4 pg/mL, p < 0.001). Skeletal muscle MOTS-c expression was also reduced in the PCOS group (74.2 ± 15.2 vs. 100.0 ± 8.5 arbitrary units; p = 0.005). Serum MOTS-c levels were inversely associated with total testosterone (r = − 0.224, p = 0.046) and total cholesterol (r = − 0.228, p = 0.044). Women with PCOS display reduced MOTS-c expression in both the circulation and skeletal muscle, suggesting reduced availability of this mitochondrial-derived peptide. Associations with hyperandrogenism and lipid profiles suggest a potential link between altered mitochondrial peptide biology and the endocrine–metabolic phenotype of PCOS. These findings suggest that MOTS-c may represent a potential marker of tissue-specific mitochondrial involvement in PCOS and warrant further investigation.