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棕榈油酸慢性给药可降低遗传性 2 型糖尿病 KK-Ay 小鼠的胰岛素抵抗和肝脏脂质蓄积。

Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes.

机构信息

Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo 192-0991, Japan.

出版信息

Lipids Health Dis. 2011 Jul 21;10:120. doi: 10.1186/1476-511X-10-120.

DOI:10.1186/1476-511X-10-120
PMID:21774832
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3155149/
Abstract

BACKGROUND

Studies have demonstrated the beneficial effect of palmitoleic acid (C16:1 n-7) on reducing muscle insulin resistance and preventing beta-cell apoptosis. However, the effect of palmitoleic acid on diabetes remains to be elucidated. The aim of this study was to examine the antidiabetic effect of palmitoleic acid in KK-Ay mice, a spontaneous model for studies of obese type 2 diabetes with low insulin sensitivity.

METHODS

KK-Ay mice were orally administered vehicle, 300 mg/kg of palmitoleic acid, or 300 mg/kg of palmitic acid (C16:0) on a daily basis for 4 weeks.

RESULTS

Palmitoleic acid reduced body weight increase, ameliorated the development of hyperglycemia and hypertriglyceridemia, and improved insulin sensitivity. In addition, hepatic characteristics were significantly affected, as weight of the liver and hepatic triglyceride levels were lower in the palmitoleic acid group when compared to the control (vehicle and palmitic acid groups). Oil red O staining clearly indicated reduced hepatic lipid accumulation in response to palmitoleic acid. Furthermore, palmitoleic acid down-regulated mRNA expressions of proinflammatory adipocytokine genes (TNFα and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver.

CONCLUSIONS

These results suggest that palmitoleic acid improves hyperglycemia and hypertriglyceridemia by increasing insulin sensitivity, in part owing to suppressing proinflammatory gene expressions and improving hepatic lipid metabolism in diabetic mice.

摘要

背景

研究表明，棕榈油酸（C16:1n-7）有益于降低肌肉胰岛素抵抗和预防β细胞凋亡。然而，棕榈油酸对糖尿病的影响仍需阐明。本研究旨在观察棕榈油酸对 KK-Ay 小鼠（一种肥胖 2 型糖尿病伴胰岛素敏感性降低的自发性模型）的抗糖尿病作用。

方法

KK-Ay 小鼠每天经口给予载体、300mg/kg 棕榈油酸或 300mg/kg 棕榈酸（C16:0），连续 4 周。

结果

棕榈油酸可减少体重增加，改善高血糖和高三酰甘油血症的发展，并提高胰岛素敏感性。此外，肝脏特征也受到显著影响，与对照组（载体和棕榈酸组）相比，棕榈油酸组的肝脏重量和肝三酰甘油水平较低。油红 O 染色清楚地表明，肝脏脂质蓄积减少。此外，棕榈油酸下调了白色脂肪组织中促炎脂肪细胞因子基因（TNFα和抵抗素）和肝脏中脂肪生成基因（SREBP-1、FAS 和 SCD-1）的 mRNA 表达。

结论

这些结果表明，棕榈油酸通过增加胰岛素敏感性改善高血糖和高三酰甘油血症，部分原因是抑制促炎基因表达和改善糖尿病小鼠的肝脏脂质代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/57d8fda2a645/1476-511X-10-120-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/6eb6f2338439/1476-511X-10-120-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/b48d3de9868d/1476-511X-10-120-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/0b24d47d0756/1476-511X-10-120-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/8f98d5bce32f/1476-511X-10-120-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/57d8fda2a645/1476-511X-10-120-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/6eb6f2338439/1476-511X-10-120-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/b48d3de9868d/1476-511X-10-120-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/0b24d47d0756/1476-511X-10-120-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/8f98d5bce32f/1476-511X-10-120-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4640/3155149/57d8fda2a645/1476-511X-10-120-5.jpg

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