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丁酸盐可改善母源性高脂肪饮食诱导的胎肝细胞凋亡。

Butyrate ameliorates maternal high-fat diet-induced fetal liver cellular apoptosis.

机构信息

Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Department of Family Medicine, Kaohsiung Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

出版信息

PLoS One. 2022 Jul 6;17(7):e0270657. doi: 10.1371/journal.pone.0270657. eCollection 2022.

DOI:10.1371/journal.pone.0270657
PMID:35793323
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9258878/
Abstract

A maternal high-fat diet (HFD) can impact the offspring's development of liver steatosis, with fetal development in utero being a crucial period. Therefore, this study investigated the mechanism and whether butyrate can rescue liver injury caused by maternal HFD in the fetus. Pregnant female Sprague Dawley rats were randomly divided into two groups, prenatal HFD (58% fat) exposure or normal control diet (4.5% fat). The HFD group was fed an HFD 7 weeks before mating and during gestation until sacrifice at gestation 21 days. After confirmation of mating, the other HFD group was supplemented with sodium butyrate (HFSB). The results showed that maternal liver histology showed lipid accumulation with steatosis and shortened ileum villi in HFD, which was ameliorated in the HFSB group (P<0.05). There was increased fetal liver and ileum TUNEL staining and IL-6 expression with increased fetal liver TNF-α and malondialdehyde expression in the HFD group (P<0.05), which decreased in the HFSB group (P<0.05). The fetal liver expression of phospho-AKT/AKT and GPX1 decreased in the HFD group but increased in the HFSB group (P<0.05). In conclusion that oxidative stress with inflammation and apoptosis plays a vital role after maternal HFD in the fetus liver that can be ameliorated with butyrate supplementation.

摘要

高脂肪饮食可影响后代肝脏脂肪变性的发生,而胎儿在子宫内的发育是一个关键时期。因此,本研究探讨了母体高脂肪饮食(HFD)导致胎儿肝脏损伤的机制,以及丁酸盐是否可以对此进行挽救。将怀孕的雌性 Sprague Dawley 大鼠随机分为两组,即产前 HFD(58%脂肪)暴露或正常对照饮食(4.5%脂肪)组。HFD 组在交配前 7 周开始摄入 HFD,并在妊娠期间持续喂养至妊娠第 21 天处死。确认交配后,另一个 HFD 组补充丁酸钠(HFSB)。结果显示,HFD 组母鼠肝脏组织学显示出脂肪堆积和脂肪变性,回肠绒毛变短,而 HFSB 组则有所改善(P<0.05)。HFD 组胎肝和回肠 TUNEL 染色以及 IL-6 表达增加,胎肝 TNF-α和丙二醛表达增加(P<0.05),而 HFSB 组则减少(P<0.05)。HFD 组胎肝磷酸化 AKT/AKT 和 GPX1 表达降低,但 HFSB 组增加(P<0.05)。总之,母体 HFD 后胎儿肝脏中的氧化应激、炎症和细胞凋亡起着至关重要的作用,而丁酸盐的补充可以对此进行改善。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/a90f32cdb811/pone.0270657.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/fa27e39097e3/pone.0270657.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/ef32dda83aec/pone.0270657.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/c85f73c30987/pone.0270657.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/e5ed1b98cc0e/pone.0270657.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/8eff7c26bfa4/pone.0270657.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/a90f32cdb811/pone.0270657.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/fa27e39097e3/pone.0270657.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/ef32dda83aec/pone.0270657.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/c85f73c30987/pone.0270657.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/e5ed1b98cc0e/pone.0270657.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/8eff7c26bfa4/pone.0270657.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7569/9258878/a90f32cdb811/pone.0270657.g006.jpg

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