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首页> 外文期刊>American Journal of Physiology >Betaine improves nonalcoholic fatty liver and associated hepatic insulin resistance: a potential mechanism for hepatoprotection by betaine.
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Betaine improves nonalcoholic fatty liver and associated hepatic insulin resistance: a potential mechanism for hepatoprotection by betaine.

机译：甜菜碱可改善非酒精性脂肪肝及相关的肝胰岛素抵抗：甜菜碱对肝脏的保护作用潜在机制。

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摘要

Nonalcoholic fatty liver (NAFL) is a common liver disease, associated with insulin resistance. Betaine has been tested as a treatment for NAFL in animal models and in small clinical trials, with mixed results. The present study aims to determine whether betaine treatment would prevent or treat NAFL in mice and to understand how betaine reverses hepatic insulin resistance. Male mice were fed a moderate high-fat diet (mHF) containing 20% of calories from fat for 7 (mHF) or 8 (mHF8) mo without betaine, with betaine (mHFB), or with betaine for the last 6 wk (mHF8B). Control mice were fed standard chow containing 9% of calories from fat for 7 mo (SF) or 8 mo (SF8). HepG2 cells were made insulin resistant and then studied with or without betaine. mHF mice had higher body weight, fasting glucose, insulin, and triglycerides and greater hepatic fat than SF mice. Betaine reduced fasting glucose, insulin, triglycerides, and hepatic fat. In the mHF8B group, betaine treatment significantly improved insulin resistance and hepatic steatosis. Hepatic betaine content significantly decreased in mHF and increased significantly in mHFB. Betaine treatment reversed the inhibition of hepatic insulin signaling in mHF and in insulin-resistant HepG2 cells, including normalization of insulin receptor substrate 1 (IRS1) phosphorylation and of downstream signaling pathways for gluconeogenesis and glycogen synthesis. Betaine treatment prevents and treats fatty liver in a moderate high-dietary-fat model of NAFL in mice. Betaine also reverses hepatic insulin resistance in part by increasing the activation of IRS1, with resultant improvement in downstream signaling pathways.
机译：非酒精性脂肪肝（NAFL）是常见的肝脏疾病，与胰岛素抵抗有关。甜菜碱已经在动物模型和小型临床试验中作为NAFL的治疗剂进行了测试，结果不一。本研究旨在确定甜菜碱治疗是否会预防或治疗小鼠NAFL，并了解甜菜碱如何逆转肝胰岛素抵抗。给雄性小鼠喂食中度高脂饮食（mHF），其中7％（mHF）或8（mHF8）个月的脂肪含20％的卡路里，不含甜菜碱，甜菜碱（mHFB）或最后6周含甜菜碱（mHF8B） ）。对照小鼠饲喂标准脂肪，其中脂肪中含有9％的卡路里，持续7 mo（SF）或8 mo（SF8）。使HepG2细胞具有胰岛素抵抗性，然后在有或没有甜菜碱的情况下进行研究。与SF小鼠相比，mHF小鼠具有更高的体重，空腹血糖，胰岛素和甘油三酸酯以及更高的肝脂肪。甜菜碱可降低空腹血糖，胰岛素，甘油三酸酯和肝脂肪。在mHF8B组中，甜菜碱治疗可显着改善胰岛素抵抗和肝脂肪变性。肝甜菜碱含量在mHF中显着降低，在mHFB中显着提高。甜菜碱治疗逆转了mHF和胰岛素抵抗性HepG2细胞中对肝胰岛素信号的抑制作用，包括胰岛素受体底物1（IRS1）磷酸化的正常化以及糖异生和糖原合成的下游信号通路的正常化。甜菜碱治疗可预防和治疗小鼠中度NAF高脂肪饮食模型中的脂肪肝。甜菜碱还可以通过增加IRS1的激活来部分逆转肝胰岛素抵抗，从而改善下游信号通路。

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