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Metformin ameliorates maternal high-fat diet-induced maternal dysbiosis and fetal liver apoptosis
Lipids in Health and Disease ( IF 4.5 ) Pub Date : 2021-09-08 , DOI: 10.1186/s12944-021-01521-w
Szu-Wei Huang , Yu-Che Ou , Kuo-Shu Tang , Hong-Ren Yu , Li-Tung Huang , You-Lin Tain , I-Chun Lin , Jiunn-Ming Sheen , Chih-Yao Hou , Ching-Chou Tsai , Mao-Meng Tiao

The deleterious effect of maternal high-fat diet (HFD) on the fetal rat liver may cause later development of non-alcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the effect of maternal HFD-induced maternal hepatic steatosis and dysbiosis on the fetal liver and intestines, and the effect of prenatal metformin in a rat model. Sprague–Dawley rats were assigned to three groups (N = 6 in each group). Before mating, the rats were randomly assigned to HFD or normal-chow diet (NCD) group for 7 weeks. After mating, the HFD group rats were continued with high-fat diet during pregnancy and some of the HFD group rats were co-treated with metformin (HFMf) via drinking water during pregnancy. All maternal rats and their fetuses were sacrificed on gestational day 21. The liver and intestinal tissues of both maternal and fetal rats were analyzed. In addition, microbial deoxyribonucleic acid extracted from the maternal fecal samples was analyzed. HFD resulted in maternal weight gain during pregnancy, intrahepatic lipid accumulation, and change in the serum short-chain fatty acid profile, intestinal tight junctions, and dysbiosis in maternal rats. The effect of HFD on maternal rats was alleviated by prenatal metformin, which also ameliorated inflammation and apoptosis in the fetal liver and intestines. This study demonstrated the beneficial effects of prenatal metformin on maternal liver steatosis, focusing on the gut-liver axis. In addition, the present study indicates that prenatal metformin could ameliorate maternal HFD-induced inflammation and apoptosis in the fetal liver and intestines. This beneficial effect of in-utero exposure of metformin on fetal liver and intestines has not been reported. This study supports the use of prenatal metformin for pregnant obese women.

中文翻译:

二甲双胍改善母体高脂饮食诱导的母体生态失调和胎儿肝细胞凋亡

母体高脂饮食 (HFD) 对胎鼠肝脏的有害影响可能会导致以后发展为非酒精性脂肪肝病 (NAFLD)。本研究的目的是评估母体 HFD 诱导的母体肝脏脂肪变性和生态失调对胎儿肝脏和肠道的影响,以及产前二甲双胍在大鼠模型中的影响。Sprague-Dawley 大鼠被分为三组(每组 N = 6)。在交配前,将大鼠随机分配到HFD或正常饮食(NCD)组7周。交配后,HFD组大鼠在孕期继续高脂饮食,部分HFD组大鼠在孕期通过饮水给予二甲双胍(HFMf)联合治疗。在妊娠第 21 天处死所有母鼠及其胎儿。分析了母鼠和胎鼠的肝脏和肠组织。此外,还分析了从母体粪便样品中提取的微生物脱氧核糖核酸。HFD 导致母鼠在怀孕期间体重增加、肝内脂质积累、血清短链脂肪酸谱的变化、肠道紧密连接和母鼠的生态失调。产前二甲双胍减轻了 HFD 对母鼠的影响,这也改善了胎儿肝脏和肠道的炎症和细胞凋亡。这项研究证明了产前二甲双胍对母体肝脏脂肪变性的有益作用,重点是肠-肝轴。此外,本研究表明产前二甲双胍可以改善母体 HFD 诱导的胎儿肝脏和肠道炎症和细胞凋亡。子宫内暴露二甲双胍对胎儿肝脏和肠道的这种有益作用尚未见报道。该研究支持对妊娠肥胖妇女使用产前二甲双胍。
更新日期:2021-09-08
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