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低脂饮食对非酒精性脂肪性肝病大鼠肝脏脂联素及其受体表达的影响。

Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD.

作者信息

Ma Hong, You Guo-Ping, Cui Fan, Chen Lu-Fang, Yang Xiang-Jiu, Chen Li-Gang, Lu Hua-Dong, Zhang Wen-Qiang

机构信息

Departments of Endocrinology, Zhongshan Hospital Xiamen University, Fujian, China.

Department of Endocrinology, Xiamen Zhongshan Teaching Hospital of Fujian Medical University, Fujian, China.

出版信息

Ann Hepatol. 2015 Jan-Feb;14(1):108-17.

Abstract

BACKGROUND

Non-alcoholic fatty liver disease (NAFLD) is correlated with obesity, but specific therapeutic interventions are lacking. Adiponectin is an adipokine with anti-inflammatory activity and is considered a hepatic protector. We aimed to investigate effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD.

MATERIALS AND METHODS

Sixteen male SD rats were fed a high-fat diet for 8 weeks (HFD1 group) or 16 weeks (HFD2 group) to induce NAFLD, and these rats were compared with rats on a normal diet for 8 weeks (NC1 group) or 16 weeks (NC2 group). Another group of 8 rats was fed an HFD for 8 weeks and then switched to a low-fat diet (DIET group) until the 16th week. The expression of hepatic adiponectin and its receptors was detected by western blotting, immunohistochemistry and RT-qPCR.

RESULTS

The NAFLD activity score (NAS) in the HFD groups increased from 3.2 ± 0.45 (8th week) to 6.2 ± 0.84 (16th week) (P < 0.001), reflecting the progression in the NAFLD histology. In contrast to the HFD2 group, the low-fat diet ameliorated the steatosis, ballooning degeneration and inflammation. Dietary intervention augmented the expression of adiponectin and its receptors, which was down-regulated in the HFD2 group.

CONCLUSIONS

The NAFLD rat model was successfully developed by feeding the animals a high-fat diet. Adiponectin may play a role in the pathogenesis of NAFLD, especially in the progression from steatosis to NASH. The low-fat diet alleviated the histological lesions associated with NAFLD by up-regulating the expression of adiponectin and its receptors.

摘要

背景

非酒精性脂肪性肝病(NAFLD)与肥胖相关,但缺乏特异性治疗干预措施。脂联素是一种具有抗炎活性的脂肪因子,被认为是肝脏保护因子。我们旨在研究低脂饮食对NAFLD大鼠肝脏脂联素及其受体表达的影响。

材料与方法

16只雄性SD大鼠分别给予高脂饮食8周(HFD1组)或16周(HFD2组)以诱导NAFLD,并将这些大鼠与给予正常饮食8周(NC1组)或16周(NC2组)的大鼠进行比较。另一组8只大鼠给予高脂饮食8周,然后改为低脂饮食(饮食组)直至第16周。通过蛋白质免疫印迹法、免疫组织化学和逆转录-定量聚合酶链反应检测肝脏脂联素及其受体的表达。

结果

HFD组的NAFLD活动评分(NAS)从3.2±0.45(第8周)增加到6.2±0.84(第16周)(P<0.001),反映了NAFLD组织学的进展。与HFD2组相比,低脂饮食改善了脂肪变性、气球样变性和炎症。饮食干预增加了脂联素及其受体的表达,而在HFD2组中其表达下调。

结论

通过给动物喂食高脂饮食成功建立了NAFLD大鼠模型。脂联素可能在NAFLD的发病机制中起作用,尤其是在从脂肪变性到非酒精性脂肪性肝炎的进展过程中。低脂饮食通过上调脂联素及其受体的表达减轻了与NAFLD相关的组织学病变。

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