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左旋肉碱对肥胖糖尿病小鼠的心脏保护作用:心脏和脂肪组织中 Chemerin 和 CMKLRI 表达的调节。

Novel Cardioprotective Effect of L-Carnitine on Obese Diabetic Mice: Regulation of Chemerin and CMKLRI Expression in Heart and Adipose Tissues.

机构信息

Department of Basic Sciences, Division of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz - Irã.

Department of Nutrition Science, Ahvaz Jundishapur University of Medical Sciences, Ahvaz - Irã.

出版信息

Arq Bras Cardiol. 2021 Oct;117(4):715-725. doi: 10.36660/abc.20200044.

DOI:10.36660/abc.20200044
PMID:34709299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8528366/
Abstract

BACKGROUND

L-carnitine (LC) has many beneficial effects on diabetic animals and humans, but its regulatory effect on chemerin as an inflammatory cytokine, and its receptor in diabetes status is unknown.

OBJECTIVES

The present study aimed to investigate the regulatory effect of LC on the expression of chemerin and chemokine-like receptor I (CMKLRI) in adipose and cardiac tissues of diabetic mice.

METHODS

Sixty NMARI mice were divided into four groups including control, diabetic, diabetic + LC supplementation and control + LC supplementation. Diabetes was induced by feeding the animals a high-calorie diet for 5 weeks and injection of Streptozotocin. The animals were treated with 300 mg/kg LC for 28 days. On days 7, 14, and 28 after treatment, the mRNA and protein levels of chemerin and CMKLRI in the cardiac and adipose tissues of the animals were determined using qPCR analysis and ELISA. Insulin resistance indices were also measured in all experimental groups. Differences with p <0.05 were considered significant.

RESULTS

Chemerin and CMKLRI expressions levels were increased in cardiac and adipose tissues of diabetic mice on days 14 and 28 after diabetes induction, concurrent with the incidence of insulin resistance and increased levels of circulating chemerin (p<0.05). The treatment with LC caused a significant decrease in the expression of both genes in studied tissues and the reduction of insulin resistance symptoms and serum chemerin levels (p<0.05).

CONCLUSION

The results suggest that LC treatment were able to downregulate the expression of chemerin and CKLR1 in cardiac and adipose tissues of obese, diabetic experimental animals.

摘要

背景

左旋肉碱(LC)对糖尿病动物和人类有许多有益的影响,但它对趋化素作为炎症细胞因子的调节作用及其在糖尿病状态下的受体尚不清楚。

目的

本研究旨在探讨 LC 对糖尿病小鼠脂肪和心脏组织中趋化素和趋化因子样受体 I(CMKLRI)表达的调节作用。

方法

将 60 只 NMARI 小鼠分为对照组、糖尿病组、糖尿病+LC 补充组和对照组+LC 补充组四组。通过给予动物高热量饮食 5 周和链脲佐菌素注射诱导糖尿病。动物用 300mg/kg LC 治疗 28 天。在治疗后第 7、14 和 28 天,通过 qPCR 分析和 ELISA 测定动物心脏和脂肪组织中趋化素和 CMKLRI 的 mRNA 和蛋白水平。还测量了所有实验组的胰岛素抵抗指数。差异具有统计学意义(p<0.05)。

结果

糖尿病诱导后第 14 和 28 天,糖尿病小鼠心脏和脂肪组织中趋化素和 CMKLRI 的表达水平升高,同时出现胰岛素抵抗和循环趋化素水平升高(p<0.05)。LC 治疗可显著降低研究组织中这两个基因的表达,减轻胰岛素抵抗症状和血清趋化素水平(p<0.05)。

结论

结果表明,LC 治疗可下调肥胖、糖尿病实验动物心脏和脂肪组织中趋化素和 CKLR1 的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/e786af7ca4e7/0066-782X-abc-117-04-0715-gf05-en.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/0a3c39736b8e/0066-782X-abc-117-04-0715-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/8a479547e03c/0066-782X-abc-117-04-0715-gf01-en.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/e786af7ca4e7/0066-782X-abc-117-04-0715-gf05-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/9f3f77658f80/0066-782X-abc-117-04-0715-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/7a320eabc567/0066-782X-abc-117-04-0715-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/e29e02d6ad4d/0066-782X-abc-117-04-0715-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/7c080ada9510/0066-782X-abc-117-04-0715-gf04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/0a3c39736b8e/0066-782X-abc-117-04-0715-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/8a479547e03c/0066-782X-abc-117-04-0715-gf01-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/7b78f5c5812f/0066-782X-abc-117-04-0715-gf02-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/8cd9fa889a75/0066-782X-abc-117-04-0715-gf03-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/850590b98f07/0066-782X-abc-117-04-0715-gf04-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/802a/8528366/e786af7ca4e7/0066-782X-abc-117-04-0715-gf05-en.jpg

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