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<p>This study examined the potential role of TGF-β/Smad signaling in mediating the concurrent impact of hypothyroid with obesity on sperm and testicular functions. Hypothyroidism was induced by methimazole treatment to adult ICR male mice followed by high-fat diet (HFD) feeding resulting obesity. Other groups were obese or hypothyroid. Mice with hypothyroidism and/or obesity were sacrificed, and blood was obtained via cardiac-puncture. Testes were harvested and sperm were collected from cauda epididymis. Serum testosterone levels were reduced while serum leptin, LH and FSH levels were increased in hypothyroid with obesity mice (<i>p</i> &lt; 0.05) compared to hypothyroid or obesity alone. Hypothyroid with obesity mice had a significant decline in testicular microarchitecture, including downregulation of spermatogenesis-related proteins (e.g., connexin43, N-cadherin, occludin, JAM-A, AR, Sirt1, SOX9, vimentin, GATA4) and steroidogenic proteins (e.g., StAR, Cyp17a1, Hsd17β1, and Smad proteins. Additionally, mice with concomitant hypothyroidism with obesity have higher percentage of abnormal sperm, sperm with fragmented DNA, but lower sperm count, motility, vitality, and hypo-osmotic swelling (HOS) positive sperm (<i>p</i> &lt; 0.05) compared to hypothyroid or obesity alone. Altered sperm parameters were associated with downregulation of sperm PAWP, phospho-tyrosine, and Smad protein (Smad2 and Smad4) expression. In conclusion hypothyroidism with obesity accentuate testicular and sperm dysfunctions which might involve TGFβ/Smad signaling.</p>

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Concomitant Effect of Hypothyroidism with Obesity on Testicular and Sperm Function in Male ICR Mice: Involvement of TGFβ/SMAD Signaling

  • 期刊论文

  • 发表日期：

    2025年12月30日

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  • Madhumanti Barman,
  • Giribabu Nelli,
  • Sabyasachi Das,
  • Naguib Salleh

摘要

This study examined the potential role of TGF-β/Smad signaling in mediating the concurrent impact of hypothyroid with obesity on sperm and testicular functions. Hypothyroidism was induced by methimazole treatment to adult ICR male mice followed by high-fat diet (HFD) feeding resulting obesity. Other groups were obese or hypothyroid. Mice with hypothyroidism and/or obesity were sacrificed, and blood was obtained via cardiac-puncture. Testes were harvested and sperm were collected from cauda epididymis. Serum testosterone levels were reduced while serum leptin, LH and FSH levels were increased in hypothyroid with obesity mice (p < 0.05) compared to hypothyroid or obesity alone. Hypothyroid with obesity mice had a significant decline in testicular microarchitecture, including downregulation of spermatogenesis-related proteins (e.g., connexin43, N-cadherin, occludin, JAM-A, AR, Sirt1, SOX9, vimentin, GATA4) and steroidogenic proteins (e.g., StAR, Cyp17a1, Hsd17β1, and Smad proteins. Additionally, mice with concomitant hypothyroidism with obesity have higher percentage of abnormal sperm, sperm with fragmented DNA, but lower sperm count, motility, vitality, and hypo-osmotic swelling (HOS) positive sperm (p < 0.05) compared to hypothyroid or obesity alone. Altered sperm parameters were associated with downregulation of sperm PAWP, phospho-tyrosine, and Smad protein (Smad2 and Smad4) expression. In conclusion hypothyroidism with obesity accentuate testicular and sperm dysfunctions which might involve TGFβ/Smad signaling.