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非靶向代谢组学揭示肥胖症中下降的 PE 和 PC 可能与前列腺增生有关。

Untargeted metabolomics reveals that declined PE and PC in obesity may be associated with prostate hyperplasia.

机构信息

Clinical Medical College, North China University of Science and Technology, Tangshan, China.

School of Public Health, North China University of Science and Technology, Tangshan, China.

出版信息

PLoS One. 2024 Apr 19;19(4):e0301011. doi: 10.1371/journal.pone.0301011. eCollection 2024.

DOI:10.1371/journal.pone.0301011
PMID:38640132
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11029648/
Abstract

BACKGROUND

Recent studies have shown that obesity may contribute to the pathogenesis of benign prostatic hyperplasia (BPH). However, the mechanism of this pathogenesis is not fully understood.

METHODS

A prospective case-control study was conducted with 30 obese and 30 nonobese patients with BPH. Prostate tissues were collected and analyzed using ultra performance liquid chromatography ion mobility coupled with quadrupole time-of-flight mass spectrometry (UPLC-IMS-Q-TOF).

RESULTS

A total of 17 differential metabolites (3 upregulated and 14 downregulated) were identified between the obese and nonobese patients with BPH. Topological pathway analysis indicated that glycerophospholipid (GP) metabolism was the most important metabolic pathway involved in BPH pathogenesis. Seven metabolites were enriched in the GP metabolic pathway. lysoPC (P16:0/0:0), PE (20:0/20:0), PE (24:1(15Z)/18:0), PC (24:1(15Z)/14:0), PC (15:0/24:0), PE (24:0/18:0), and PC (16:0/18:3(9Z,12Z,15Z)) were all significantly downregulated in the obesity group, and the area under the curve (AUC) of LysoPC (P-16:0/0/0:0) was 0.9922. The inclusion of the seven differential metabolites in a joint prediction model had an AUC of 0.9956. Thus, both LysoPC (P-16:0/0/0:0) alone and the joint prediction model demonstrated good predictive ability for obesity-induced BPH mechanisms.

CONCLUSIONS

In conclusion, obese patients with BPH had a unique metabolic profile, and alterations in PE and PC in these patients be associated with the development and progression of BPH.

摘要

背景

最近的研究表明，肥胖可能导致良性前列腺增生（BPH）的发病机制。然而，这种发病机制的机制尚不完全清楚。

方法

对 30 例肥胖和 30 例非肥胖的 BPH 患者进行了前瞻性病例对照研究。使用超高效液相色谱离子淌度与四极杆飞行时间质谱联用（UPLC-IMS-Q-TOF）对前列腺组织进行了收集和分析。

结果

肥胖和非肥胖的 BPH 患者之间共鉴定出 17 种差异代谢物（上调 3 种，下调 14 种）。拓扑通路分析表明，甘油磷脂（GP）代谢是与 BPH 发病机制相关的最重要的代谢通路。GP 代谢途径中有 7 种代谢物富集。溶血磷脂酰胆碱（P16:0/0:0）、PE（20:0/20:0）、PE（24:1（15Z）/18:0）、PC（24:1（15Z）/14:0）、PC（15:0/24:0）、PE（24:0/18:0）和 PC（16:0/18:3（9Z，12Z，15Z））在肥胖组中均显著下调，LysoPC（P-16:0/0/0:0）的曲线下面积（AUC）为 0.9922。在联合预测模型中纳入这 7 种差异代谢物的 AUC 为 0.9956。因此，LysoPC（P-16:0/0/0:0）单独和联合预测模型均对肥胖诱导的 BPH 机制具有良好的预测能力。

结论

总之，肥胖的 BPH 患者具有独特的代谢特征，这些患者的 PE 和 PC 的改变可能与 BPH 的发生和发展有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/a33bcf5c6d3f/pone.0301011.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/4202adbc1d5c/pone.0301011.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/d03187dab473/pone.0301011.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/6047ac7ccd5f/pone.0301011.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/ceb9576ecf91/pone.0301011.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/b07a53fd821e/pone.0301011.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/a33bcf5c6d3f/pone.0301011.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/4202adbc1d5c/pone.0301011.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/d03187dab473/pone.0301011.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/6047ac7ccd5f/pone.0301011.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/ceb9576ecf91/pone.0301011.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/b07a53fd821e/pone.0301011.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1fcc/11029648/a33bcf5c6d3f/pone.0301011.g006.jpg

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