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饲用黄连素可改善高糖膳食下团头鲂糖代谢紊乱。

Dietary berberine can ameliorate glucose metabolism disorder of Megalobrama amblycephala exposed to a high-carbohydrate diet.

机构信息

Key Laboratory of Aquatic Nutrition and Feed Science of Jiangsu Province, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.

Tongwei Company Limited, No. 588 Middle Section of Tianfu Avenue, Chengdu Hi-Tech Zone, Chengdu, 610041, China.

出版信息

Fish Physiol Biochem. 2021 Apr;47(2):499-513. doi: 10.1007/s10695-021-00927-8. Epub 2021 Jan 26.

DOI:10.1007/s10695-021-00927-8
PMID:33501601
Abstract

Blunt snout bream (Megalobrama amblycephala) were randomly assigned into three diets: normal-carbohydrate diet (NCD, 30% carbohydrate, w/w), high-carbohydrate diet (HCD, 43% carbohydrate), and HCB (HCD supplemented with 50 mg/kg berberine (BBR)). After 10 weeks' feeding trial, the results showed that higher levels of plasma glucose, triglyceride, and total cholesterol were observed in HCD-fed fish than in NCD-fed fish, while HCB feeding significantly ameliorated this effect. Moreover, HCB feeding remarkably reversed HCD-induced hepatic glycogen and lipid contents. In insulin signaling, BBR inclusion restored HCD-induced suppression of insulin receptor substrate mRNA expression and elevation of forkhead transcription factor 1 mRNA expression. In glucose metabolism, upregulated glucose transporter 2 and glycogen synthase mRNA expressions in the HCD group were observed compared to the NCD group. However, BBR adding reduced the mRNA expressions of glycogen synthase, phosphoenolpyruvate carboxykinase, and glucose-6-phosphatase and increased the transcriptional levels of glucose transporter 2 and pyruvate kinase. In lipid metabolism, BBR supplementation could reverse downregulated hepatic carnitine palmitoyl transferase I mRNA expression and upregulated hepatic acetyl-CoA carboxylase and fatty acid synthetase mRNA expressions in the HCD group. Taken together, it demonstrates that BBR could improve glucose metabolism of this species via enhancing liver's glycolysis and insulin signaling, while inhibiting liver's glycogen synthesis and gluconeogenesis. It also indicates that BBR could reduce the metabolic burden of the liver by inhibiting fat synthesis and promoting lipid decomposition, and then enhance fat uptake in peripheral tissues.

摘要

圆吻鲴随机分为三组

正常碳水化合物饮食组(NCD,30%碳水化合物,w/w)、高碳水化合物饮食组(HCD,43%碳水化合物)和 HCB(HCD 补充 50mg/kg 黄连素(BBR))。10 周饲养试验结果表明,HCD 组鱼的血浆葡萄糖、甘油三酯和总胆固醇水平高于 NCD 组,而 HCB 喂养可显著改善这种情况。此外,HCB 喂养可显著逆转 HCD 诱导的肝糖原和脂质含量增加。在胰岛素信号通路中,添加 BBR 可恢复 HCD 诱导的胰岛素受体底物 mRNA 表达抑制和叉头转录因子 1 mRNA 表达升高。在葡萄糖代谢中,与 NCD 组相比,HCD 组葡萄糖转运蛋白 2 和糖原合成酶 mRNA 表达上调。然而,添加 BBR 可降低糖原合成酶、磷酸烯醇丙酮酸羧激酶和葡萄糖-6-磷酸酶的 mRNA 表达,并增加葡萄糖转运蛋白 2 和丙酮酸激酶的转录水平。在脂质代谢中,BBR 补充可逆转 HCD 组肝肉毒碱棕榈酰转移酶 I mRNA 表达下调和肝乙酰辅酶 A 羧化酶和脂肪酸合成酶 mRNA 表达上调。综上所述,BBR 可通过增强肝脏糖酵解和胰岛素信号通路,同时抑制肝脏糖原合成和糖异生,改善该物种的葡萄糖代谢。它还表明,BBR 可通过抑制脂肪合成和促进脂质分解来减轻肝脏的代谢负担,然后增强外周组织的脂肪摄取。

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