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RBP4 的异位表达会损害小鼠的胰岛素通路和腹股沟脂肪沉积。

Ectopic expression of RBP4 impairs the insulin pathway and inguinal fat deposition in mice.

机构信息

College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.

出版信息

J Physiol Biochem. 2014 Jun;70(2):479-86. doi: 10.1007/s13105-014-0326-3. Epub 2014 Mar 4.

Abstract

A large body of evidence has linked retinol-binding protein 4 (RBP4) to systemic insulin resistance, but little is known about its function in fat deposition. This study aimed to confirm the involvement of RBP4 in inguinal fat deposition and insulin by intraperitoneal injection of adenovirus-mediated RBP4 to mice. Intraperitoneal injection of adenoviral vectors was validated as an efficient gene manipulation tool for over-expressing recombinant proteins in vivo. Ectopic expression of RBP4 decelerated inguinal fat deposition by decreasing the size of adipocytes. Moreover, the introduction of exogenous RBP4 blunted the response of inguinal adipocytes to insulin signals. These findings suggest that RBP4 impaired in vivo adipogenesis, partly through the repression of the insulin pathway.

摘要

大量证据表明视黄醇结合蛋白 4(RBP4)与全身胰岛素抵抗有关,但对于其在脂肪沉积中的作用知之甚少。本研究旨在通过腹腔注射腺病毒介导的 RBP4 来确认 RBP4 参与腹股沟脂肪沉积和胰岛素的作用。腹腔内注射腺病毒载体被验证为一种有效的体内过表达重组蛋白的基因操作工具。RBP4 的异位表达通过减小脂肪细胞的大小来减缓腹股沟脂肪的沉积。此外,外源性 RBP4 的引入削弱了腹股沟脂肪细胞对胰岛素信号的反应。这些发现表明,RBP4 通过抑制胰岛素通路损害体内脂肪生成。

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