Published online Nov 15, 2022. doi: 10.4239/wjd.v13.i11.972
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
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.
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.
To investigate the effects of dietary CML on cardiac remodeling and glucose metabolism.
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.
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.
Dietary CML promoted cardiac remodeling and abnormal glucose metabolism.
This study emphasizes the cardiac hazards of dietary CML and provides new suggestions for the diet preparation in the prevention and treatment cardiovascular diseases.