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维生素A对肥胖大鼠高密度脂蛋白胆固醇及B类清道夫受体的影响。

Impact of vitamin A on high-density lipoprotein-cholesterol and scavenger receptor class BI in the obese rat.

作者信息

Jeyakumar Shanmugam M, Vajreswari Ayyalasomayajula, Giridharan Nappan V

机构信息

Department of Biochemistry, National Institute of Nutrition, Hyderabad, India.

出版信息

Obesity (Silver Spring). 2007 Feb;15(2):322-9. doi: 10.1038/oby.2007.534.

Abstract

OBJECTIVE

Scavenger receptor class BI (SR-BI), authentic high-density lipoprotein (HDL) receptors expressed in liver, are known to play an important role in HDL-cholesterol (C) metabolism and reverse cholesterol transport. Interestingly, obese rats of WNIN/Ob strain have abnormally elevated levels of serum HDL-C compared with their lean counterparts. Based on the well-established role of SR-B1 in HDL-C metabolism, it was hypothesized that these obese rats may have an underexpression of hepatic SR-B1 receptors. In view of the significant role of vitamin A in energy expenditure and obesity, we also tested whether vitamin A supplementation can correct abnormal HDL-C metabolism.

RESEARCH METHODS AND PROCEDURES

To test this hypothesis, 7-month-old male lean and obese rats of WNIN/Ob strain were divided into two groups; each group was subdivided into two subgroups consisting of six lean and six obese rats and received diets containing either 2.6 or 129 mg vitamin A/kg diet for 2 months.

RESULTS

At the end, obese rats receiving normal levels of vitamin A diet showed high serum HDL-C and lower hepatic SR-BI expression levels compared with lean counterparts. Furthermore, chronic dietary vitamin A supplementation resulted in overexpression of hepatic SR-BI receptors (protein and gene) with concomitant reduction in serum HDL-C levels in obese rats.

DISCUSSION

Thus, our observations highlight the role of vitamin A in reverse cholesterol transport through up-regulation of hepatic SR-BI receptors and, thereby, HDL-C homeostasis in obese rats of WNIN/Ob strain.

摘要

目的

清道夫受体BI类(SR-BI)是肝脏中表达的真正的高密度脂蛋白(HDL)受体,已知其在HDL胆固醇(C)代谢和胆固醇逆向转运中起重要作用。有趣的是,WNIN/Ob品系的肥胖大鼠与瘦大鼠相比,血清HDL-C水平异常升高。基于SR-B1在HDL-C代谢中已确立的作用,推测这些肥胖大鼠可能存在肝脏SR-B1受体表达不足。鉴于维生素A在能量消耗和肥胖中的重要作用,我们还测试了补充维生素A是否能纠正异常的HDL-C代谢。

研究方法和步骤

为验证这一假设,将7个月大的WNIN/Ob品系雄性瘦大鼠和肥胖大鼠分为两组;每组再细分为两个亚组,每组包括6只瘦大鼠和6只肥胖大鼠,分别给予含2.6或129 mg维生素A/kg饲料的饲料,持续2个月。

结果

最后,与瘦大鼠相比,接受正常水平维生素A饲料的肥胖大鼠血清HDL-C水平较高,肝脏SR-BI表达水平较低。此外,长期补充膳食维生素A导致肥胖大鼠肝脏SR-BI受体(蛋白质和基因)过表达,同时血清HDL-C水平降低。

讨论

因此,我们的观察结果突出了维生素A在WNIN/Ob品系肥胖大鼠中通过上调肝脏SR-BI受体从而维持HDL-C稳态,在胆固醇逆向转运中的作用。

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