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母体补充牛磺酸可减轻母体果糖诱导的代谢和炎症失调,并部分逆转后代的不良代谢编程。

Maternal taurine supplementation attenuates maternal fructose-induced metabolic and inflammatory dysregulation and partially reverses adverse metabolic programming in offspring.

作者信息

Li M, Reynolds C M, Sloboda D M, Gray C, Vickers M H

机构信息

Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand.

Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.

出版信息

J Nutr Biochem. 2015 Mar;26(3):267-76. doi: 10.1016/j.jnutbio.2014.10.015. Epub 2014 Dec 6.

Abstract

Excessive fructose consumption is associated with insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD), and high fructose intake during pregnancy can lead to compromised fetal development in the rat. Evidence suggests that the amino acid taurine can ameliorate fructose-induced IR and NAFLD in nonpregnant animals. This study investigated the efficacy of taurine supplementation on maternal fructose-induced metabolic dysfunction and neonatal health. Time-mated Wistar rats were randomized to four groups during pregnancy and lactation: (a) control diet (CON), (b) CON supplemented with 1.5% taurine in drinking water (CT), (c) CON supplemented with fructose solution (F) and (d) F supplemented with taurine (FT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analyzed. Maternal hyperinsulinemia, increased homeostasis model assessment of IR indices and elevated proinflammatory cytokines were observed in F group and normalized in FT group. Maternal fructose-induced hepatic steatosis accompanied with increased liver weight was ameliorated with taurine supplementation. Maternal hepatic sterol regulatory element-binding protein-1c and fatty acid synthase expression was significantly increased in the F group compared to the CON, CT and FT groups. Neonatal hepatic phosphoenolpyruvate carboxykinase expression was increased in male F neonates compared to the CON, CT and FT groups and was increased in female F and FT neonates compared to CON and CT. Interleukin-1β expression was decreased in male CT and FT neonates compared to other male groups. Hepatic tumour necrosis factor receptor-1 was lower in the male FT group than the F group. These results demonstrate that maternal taurine supplementation can partially reverse fructose-induced maternal metabolic dysfunction and may ameliorate adverse developmental programming effects in offspring in a sex-specific manner.

摘要

过量摄入果糖与胰岛素抵抗(IR)和非酒精性脂肪性肝病(NAFLD)相关,孕期高果糖摄入会导致大鼠胎儿发育受损。有证据表明,氨基酸牛磺酸可改善非孕动物中果糖诱导的IR和NAFLD。本研究调查了补充牛磺酸对母体果糖诱导的代谢功能障碍和新生儿健康的影响。将孕期和哺乳期的定时交配Wistar大鼠随机分为四组:(a)对照饮食(CON),(b)饮用水中补充1.5%牛磺酸的CON(CT),(c)补充果糖溶液的CON(F)和(d)补充牛磺酸的F(FT)。分析了母体和新生儿体重、血浆细胞因子和肝脏基因表达。F组观察到母体高胰岛素血症、IR指数的稳态模型评估增加和促炎细胞因子升高,而FT组恢复正常。补充牛磺酸可改善母体果糖诱导的肝脂肪变性并伴有肝脏重量增加。与CON、CT和FT组相比,F组母体肝脏固醇调节元件结合蛋白-1c和脂肪酸合酶表达显著增加。与CON、CT和FT组相比,雄性F新生儿的肝脏磷酸烯醇丙酮酸羧激酶表达增加,与CON和CT组相比,雌性F和FT新生儿的表达增加。与其他雄性组相比,雄性CT和FT新生儿的白细胞介素-1β表达降低。雄性FT组的肝脏肿瘤坏死因子受体-1低于F组。这些结果表明,母体补充牛磺酸可部分逆转果糖诱导的母体代谢功能障碍,并可能以性别特异性方式改善后代的不良发育编程效应。

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