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壳寡糖通过降低饮食诱导肥胖大鼠内质网应激改善肥胖。

Chitosan oligosaccharide ameliorated obesity by reducing endoplasmic reticulum stress in diet-induced obese rats.

机构信息

Guangdong Engineering Research Center of Natural Products and New Drugs, Guangdong Provincial University Engineering Technology Research Center of Natural Products and Drugs, Guangdong Pharmaceutical University, Guangzhou (510006), China.

出版信息

Food Funct. 2020 Jul 1;11(7):6285-6296. doi: 10.1039/d0fo01107j. Epub 2020 Jun 30.

Abstract

OBJECTIVE

This study aimed to determine whether chitosan oligosaccharide (COST) improves overweight by reducing endoplasmic reticulum (ER) stress in the liver and liver cancer cells.

METHODS

An obesity model was established by feeding Sprague-Dawley rats (ORs) a high-fat diet (HFD) and treating them with COST for 8 weeks. A model of lipid accumulation in hepatocellular carcinoma cells was established by treating HepG2 cells with free fatty acids and COST for 24 h.

RESULTS

COST treatment of ORs reduced weight gain, inhibited adipose tissue hypertrophy and hyperplasia, and reduced the fat-to-weight ratio. COST improved dyslipidaemia, reduced liver weight and organ index, inhibited hepatic lipid accumulation, and prevented liver steatosis, and the high COST dose increased TC and TG excretion in the stool. Treatment of lipid accumulation in HepG2 cells with COST reduced lipid accumulation and TG levels. COST modulated the expression of genes related to fat metabolism and ER stress response pathway-related factors in liver tissue and HepG2 cells.

CONCLUSIONS

COST can inhibit weight gain and improve dyslipidaemia and lipid metabolism in ORs. The COST-mediated regulation of hepatic and HepG2 cell lipid metabolism might be related to inhibition of fat synthesis, acceleration of lipid oxidative catabolism and reduction in ER stress.

摘要

目的

本研究旨在探讨壳寡糖(COST)是否通过减轻肝脏和肝癌细胞中的内质网(ER)应激来改善超重。

方法

通过给予 Sprague-Dawley 大鼠(ORs)高脂肪饮食(HFD)并用 COST 处理 8 周建立肥胖模型。用游离脂肪酸和 COST 处理 HepG2 细胞 24 h 建立肝细胞癌细胞脂质积累模型。

结果

COST 处理 ORs 可减轻体重增加,抑制脂肪组织肥大和增生,降低脂肪重量比。COST 改善血脂异常,降低肝脏重量和器官指数,抑制肝内脂质堆积,防止肝脂肪变性,高剂量 COST 增加粪便中 TC 和 TG 的排泄。COST 处理 HepG2 细胞的脂质积累可减少脂质积累和 TG 水平。COST 调节肝组织和 HepG2 细胞中与脂肪代谢和 ER 应激反应途径相关因子相关的基因表达。

结论

COST 可抑制 ORs 的体重增加并改善血脂异常和脂质代谢。COST 介导的肝和 HepG2 细胞脂质代谢调节可能与抑制脂肪合成、加速脂质氧化分解和减少 ER 应激有关。

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