AI Article Synopsis

  • The study investigates how a high-fat diet (HFD) alters gut microbiota and its relationship with Ghrelin in benign prostatic hyperplasia (BPH).
  • Ghrelin levels were found to be significantly higher in both BPH mice and patients, promoting prostate cell proliferation and growth similar to testosterone propionate (TP).
  • The findings suggest that gut microbiota and Ghrelin could contribute to BPH development and may serve as potential therapeutic targets.

Article Abstract

The role of high-fat diet (HFD) induced gut microbiota alteration and Ghrelin as well as their correlation in benign prostatic hyperplasia (BPH) were explored in our study. The gut microbiota was analyzed by 16s rRNA sequencing. Ghrelin levels in serum, along with Ghrelin and Ghrelin receptor in prostate tissue of mice and patients with BPH were measured. The effect of Ghrelin on cell proliferation, apoptosis, and induction of BPH in mice was explored. Our results indicated that BPH mice have the highest ratio of Firmicutes and Bacteroidetes induced by HFD, as well as Ghrelin level in serum and prostate tissue was significantly increased compared with control. Elevated Ghrelin content in the serum and prostate tissue of BPH patients was also observed. Ghrelin promotes cell proliferation while inhibiting cell apoptosis of prostate cells. The effect of Ghrelin on enlargement of the prostate was found almost equivalent to that of testosterone propionate (TP) which may be attenuated by Ghrelin receptor antagonist YIL-781. Ghrelin could up-regulate Jak2/pJak2/Stat3/pStat3 expression and . Our results suggested that Gut microbiota may associate with Ghrelin which plays an important role in activation of Jak2/Stat3 in BPH development. Gut microbiota and Ghrelin might be pathogenic factors for BPH and could be used as a target for mediation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8264431PMC
http://dx.doi.org/10.3389/fcell.2021.615928DOI Listing

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