膳食共轭亚油酸可使Zucker糖尿病脂肪fa/fa大鼠受损的糖耐量恢复正常。

Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat.

作者信息

Houseknecht K L, Vanden Heuvel J P, Moya-Camarena S Y, Portocarrero C P, Peck L W, Nickel K P, Belury M A

机构信息

Department of Animal Sciences, Purdue University, West Lafayette, Indiana 47907, USA.

出版信息

Biochem Biophys Res Commun. 1998 Mar 27;244(3):678-82. doi: 10.1006/bbrc.1998.8303.

DOI:10.1006/bbrc.1998.8303

PMID:9535724

Abstract

Conjugated linoleic acid (CLA) is a naturally occurring fatty acid which has anti-carcinogenic and anti-atherogenic properties. CLA activates PPAR alpha in liver, and shares functional similarities to ligands of PPAR gamma, the thiazolidinediones, which are potent insulin sensitizers. We provide the first evidence that CLA is able to normalize impaired glucose tolerance and improve hyperinsulinemia in the pre-diabetic ZDF rat. Additionally, dietary CLA increased steady state levels of aP2 mRNA in adipose tissue of fatty ZDF rats compared to controls, consistent with activation of PPAR gamma. The insulin sensitizing effects of CLA are due, at least in part, to activation of PPAR gamma since increasing levels of CLA induced a dose-dependent transactivation of PPAR gamma in CV-1 cells cotransfected with PPAR gamma and PPRE X 3-luciferase reporter construct. CLA effects on glucose tolerance and glucose homeostasis indicate that dietary CLA may prove to be an important therapy for the prevention and treatment of NIDDM.

摘要

共轭亚油酸（CLA）是一种天然存在的脂肪酸，具有抗癌和抗动脉粥样硬化特性。CLA可激活肝脏中的PPARα，并且与PPARγ的配体噻唑烷二酮具有功能相似性，噻唑烷二酮是强效的胰岛素增敏剂。我们首次证明CLA能够使糖尿病前期ZDF大鼠受损的糖耐量恢复正常，并改善高胰岛素血症。此外，与对照组相比，饮食中的CLA增加了肥胖ZDF大鼠脂肪组织中aP2 mRNA的稳态水平，这与PPARγ的激活一致。CLA的胰岛素增敏作用至少部分归因于PPARγ的激活，因为在与PPARγ和PPRE X 3 - 荧光素酶报告基因构建体共转染的CV - 1细胞中，CLA水平的增加诱导了PPARγ的剂量依赖性反式激活。CLA对糖耐量和葡萄糖稳态的影响表明，饮食中的CLA可能被证明是预防和治疗非胰岛素依赖型糖尿病的重要疗法。