Wang ZQ, Sun Z. Dietary Nε-(carboxymethyl) lysine affects cardiac glucose metabolism and myocardial remodeling in mice. World J Diabetes 2022; 13(11): 972-985 [PMID: 36437860 DOI: 10.4239/wjd.v13.i11.972]
Corresponding Author of This Article
Zhen Sun, PhD, Doctor, Department of Cardiology, Affiliated Hospital of Jiangsu University, No. 438 Jiefang Road, Zhenjiang 212001, Jiangsu Province, China. 1398041019@qq.com
Research Domain of This Article
Cell Biology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Nov 15, 2022; 13(11): 972-985 Published online Nov 15, 2022. doi: 10.4239/wjd.v13.i11.972
Dietary Nε-(carboxymethyl) lysine affects cardiac glucose metabolism and myocardial remodeling in mice
Zhong-Qun Wang, Zhen Sun
Zhong-Qun Wang, Zhen Sun, Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China
Author contributions: Sun Z designed the study and wrote the manuscript; Wang ZQ performed the experiments, analyzed the data, and prepared the images; all authors edited and approved the final version of the article.
Supported bythe National Natural Science Foundation of China, No. 82070455; Natural Science Foundation of Jiangsu Province, No. BK20201225; Medical Innovation Team Project of Jiangsu Province, No. CXTDA2017010; and Research and Innovation Funding Project for College Students in Experimental Animal Center of Jiangsu University.
Institutional animal care and use committee statement: All animal experiments were approved by the Experimental Animal Use Ethics Committee of Jiangsu University.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zhen Sun, PhD, Doctor, Department of Cardiology, Affiliated Hospital of Jiangsu University, No. 438 Jiefang Road, Zhenjiang 212001, Jiangsu Province, China. 1398041019@qq.com
Received: August 16, 2022 Peer-review started: August 16, 2022 First decision: September 4, 2022 Revised: September 15, 2022 Accepted: October 11, 2022 Article in press: October 11, 2022 Published online: November 15, 2022 Processing time: 87 Days and 8.5 Hours
ARTICLE HIGHLIGHTS
Research background
Nε-(carboxymethyl)lysine (CML), a major component of advanced glycation end products, exists in the daily diet and poses a threat to health after ingestion. It is necessary to evaluate the effect of dietary CML on the heart.
Research motivation
Previous studies have confirmed that the toxic metabolite CML can cause pathological changes in a variety of tissues such as blood vessels and bones. Foodborne CML, as the main source of CML, may lead to cardiac injuries.
Research objectives
To investigate the effects of dietary CML on cardiac remodeling and glucose metabolism.
Research methods
C57 BL/6 mice received a 20-wk CML diet (1 g/kg). The body weight, fasting blood glucose, fasting insulin and serum CML levels of mice were recorded. Exogenous CML was given to establish an in vitro H9C2 cell model. Micro-positron emission tomography was used to evaluate the glucose uptake of the mouse heart. Myocardial remodeling and glucose metabolism were detected by histological/cytological staining, Western blotting, and polymerase chain reaction.
Research results
The 20 wk of CML diet could cause insulin resistance in mice and increase CML levels in serum and heart. Myocardial fibrosis, hypertrophy and apoptosis in mice were significantly aggravated after dietary CML. Moreover, dietary CML increased myocardial glucose uptake but disrupted glucose metabolism. In vitro, exogenous CML inhibited glucose metabolism-related signaling pathways and promoted H9C2 cell hypertrophy, apoptosis and collagen I expression.
Research conclusions
Dietary CML promoted cardiac remodeling and abnormal glucose metabolism.
Research perspectives
This study emphasizes the cardiac hazards of dietary CML and provides new suggestions for the diet preparation in the prevention and treatment cardiovascular diseases.
