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Spermatogenesis is the process by which haploid sperm cells are produced in the male testes. It starts with stem cells located close to the outer rim of seminiferous tubules. These spermatogonial stem cells divide asymmetrically to give rise to additional stem cells (meaning that these structures “self-renew”), as well as sperm progenitors, called spermatocytes. Importantly, this method of asymmetric mitotic division maintains a population of spermatogonial stem cells in the male...
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Maternal diet during gestation affect prostatic tissue component in SHR/Izm offspring.

Kosuke Shibamori1, Yuki Kyoda1, Tetsuya Shindo1

  • 1Department of Urology, Sapporo Medical University School of Medicine, Sapporo, Japan.

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Summary

Maternal low-protein diets promote prostate epithelial hyperplasia, while high-fat diets increase stromal growth in offspring. These findings highlight how maternal nutrition impacts prostate development and suggest potential epigenetic mechanisms.

Keywords:
DNA methylationbenign prostatic hyperplasiahigh fat dietlow protein dietmaternal dietneuroendocrine cell

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Area of Science:

  • Reproductive biology and developmental toxicology.
  • Epigenetics and disease mechanisms.

Background:

  • Maternal nutrition is linked to offspring health outcomes, potentially via epigenetic modifications.
  • Limited research exists on the maternal nutrition-benign prostatic hyperplasia (BPH) link.
  • This study investigates maternal diet effects on offspring prostate development.

Purpose of the Study:

  • To explore the association between maternal nutrition during pregnancy and benign prostatic hyperplasia (BPH) in male offspring.
  • To evaluate the impact of low-protein (LPD) and high-fat (HFD) diets on prostate development.
  • To investigate potential underlying molecular mechanisms, including gene expression and DNA methylation.

Main Methods:

  • Female spontaneously hypertensive rats were fed standard, low-protein, or high-fat diets during gestation.
  • Offspring prostates were analyzed at 48 weeks using fluorescent immunostaining (cytokeratin, vimentin, Ki-67).
  • Gene expression (microarray, RT-PCR) and DNA methylation (pyrosequencing) were assessed.

Main Results:

  • Maternal LPD led to increased ventral prostate epithelial area, associated with upregulated apoptosis inhibitors (XIAP).
  • Maternal HFD resulted in increased stromal area, linked to epithelial mesenchymal transition (EMT) markers (vimentin, TGF-beta pathway).
  • Both LPD and HFD altered gene expression related to development and cell differentiation, with increased NFκB and Smad3.

Conclusions:

  • Maternal undernutrition (LPD) promotes offspring prostate epithelial hyperplasia.
  • Maternal obesity (HFD) induces stromal growth via EMT in offspring prostate.
  • Maternal diet significantly influences offspring prostate development, potentially through epigenetic pathways.