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紫苏油高脂肪饮食可降低血清脂质但诱导胰岛素抵抗并增加大鼠肝脏脂肪酸氧化。

High-fat diet from perilla oil induces insulin resistance despite lower serum lipids and increases hepatic fatty acid oxidation in rats.

机构信息

Laboratory Animal Center of the Academy of Military Medical Science, Beijing 100071, China.

出版信息

Lipids Health Dis. 2014 Jan 15;13:15. doi: 10.1186/1476-511X-13-15.

DOI:10.1186/1476-511X-13-15
PMID:24422660
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3904189/
Abstract

BACKGROUND

The purpose of this study is to investigate the effects of a high-fat diet from perilla oil on serum lipids, hepatic lipid metabolism and insulin sensitivity.

METHODS

Male Sprague-Dawley (SD) rats were fed either a control (CT) diet or a diet high in perilla oil (HP). After 16 weeks of feeding, the serum lipids were measured, and the gene expressions involved in hepatic fatty acid oxidation and synthesis were determined. In addition, hepatic fat deposition was detected, and insulin sensitivity was evaluated by means of euglycemic-hyperinsulinemic clamp.

RESULTS

Compared with the rats in the CT group, the HP-feeding significantly decreased the levels of triglyceride (TG), total cholesterol (TCH) and HDL-cholesterol (HDL-c). HP-feeding did not change the levels of LDL-cholesterol (LDL-c), free fatty acid (FFA), intrahepatic lipids or body weight. Moreover, the HP-feeding dramatically increased the mRNA expressions of fatty acid oxidation markers (PPAR-alpha, CPT1A) and fatty acid synthesis markers (SREBP-1, FASN and ACC) in the liver. The HP-feeding induced increased protein levels of CPT1A, while reducing the protein levels of FASN and ACC in the liver. However, the glucose infusion rate significantly increased in the HP group compared with the CT group.

CONCLUSIONS

Our data show that, in rats, excessive perilla oil intake may significantly lower serum lipids, strengthen hepatic fatty acid oxidation, and inhibit hepatic fatty acid synthesis, but at the same time may also lead to insulin resistance.

摘要

背景

本研究旨在探讨紫苏油高脂饮食对血清脂质、肝脂代谢和胰岛素敏感性的影响。

方法

雄性 Sprague-Dawley(SD)大鼠分别喂食对照(CT)饮食或富含紫苏油(HP)的饮食。喂养 16 周后,检测血清脂质,并测定参与肝脂肪酸氧化和合成的基因表达。此外,检测肝脂肪沉积,通过正葡萄糖高胰岛素钳夹评估胰岛素敏感性。

结果

与 CT 组大鼠相比,HP 喂养显著降低了甘油三酯(TG)、总胆固醇(TCH)和高密度脂蛋白胆固醇(HDL-c)水平。HP 喂养并未改变 LDL-胆固醇(LDL-c)、游离脂肪酸(FFA)、肝内脂质或体重水平。此外,HP 喂养显著增加了肝脏中脂肪酸氧化标志物(PPAR-α、CPT1A)和脂肪酸合成标志物(SREBP-1、FASN 和 ACC)的 mRNA 表达。HP 喂养诱导 CPT1A 蛋白水平升高,同时降低了肝脏中 FASN 和 ACC 的蛋白水平。然而,与 CT 组相比,HP 组的葡萄糖输注率显著增加。

结论

我们的数据表明,在大鼠中,过量摄入紫苏油可能显著降低血清脂质,增强肝脂肪酸氧化,抑制肝脂肪酸合成,但同时也可能导致胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/164571941411/1476-511X-13-15-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/593a0cdaeb5b/1476-511X-13-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/05cca3385e71/1476-511X-13-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/a49c65d4810f/1476-511X-13-15-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/41da495bde46/1476-511X-13-15-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/0480915d617f/1476-511X-13-15-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/164571941411/1476-511X-13-15-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/593a0cdaeb5b/1476-511X-13-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/05cca3385e71/1476-511X-13-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/a49c65d4810f/1476-511X-13-15-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/41da495bde46/1476-511X-13-15-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/0480915d617f/1476-511X-13-15-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07df/3904189/164571941411/1476-511X-13-15-6.jpg

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