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Published on: April 3, 2017
High-Fructose Diet Induces Cardiac Dysfunction via Macrophage Recruitment in Adult Mice
Xiao Wang1,2, Zuqing Xu1,3, Rong Chang1,2
1Department of Ultrasound, Shenzhen Longhua District Central Hospital, Guangdong Medical University, Shenzhen, China.
Insights
High fructose intake significantly increases cardiomyocyte size and impairs cardiac function in mice. This diet promotes cardiac inflammation by recruiting macrophages, contributing to heart disease development.
Area of Science:
- Cardiology
- Molecular Biology
- Pathology
Background:
- Cardiovascular diseases are a leading global cause of death.
- High-fat/fructose diets contribute to metabolic syndrome, obesity, and cardiac issues like hypertrophy and fibrosis.
- Mechanisms of cardiac inflammation induced by high-fructose diets require further elucidation.
Purpose of the Study:
- To investigate the effects of a high-fructose diet on cardiac inflammation and function in mice.
- To explore the role of macrophage recruitment in high-fructose-induced cardiac injury.
Main Methods:
- Adult mice were fed a 60% high-fructose diet for 12 weeks.
- Echocardiography was used to assess cardiac function (ejection fraction, fractional shortening).
- mRNA and protein levels of inflammatory markers (MCP-1) were analyzed in cardiomyocytes and in vivo models.
Main Results:
- High-fructose diet increased cardiomyocyte size and left ventricular wall thickness.
- Cardiac function, including ejection fraction and fractional shortening, was significantly reduced.
- Increased MCP-1 levels were observed, leading to pro-inflammatory and pro-fibrotic gene expression and macrophage infiltration.
Conclusions:
- High-fructose intake induces cardiac inflammation through macrophage recruitment in cardiomyocytes.
- This inflammation contributes to impaired cardiac function and cardiac remodeling.
- The study highlights the detrimental effects of high-fructose diets on cardiovascular health.
Abstract:
Cardiovascular diseases are the leading cause of death globally, including cardiac fibrosis, myocardial infarction, cardiac hypertrophy, and heart failure. High fat/ fructose induces metabolic syndrome, hypertension and obesity, which contributes to cardiac hypertrophy and fibrosis. Excessive fructose intake accelerates inflammation in different organs and tissues, and molecular and cellular mechanisms of organ and tissue injury have been demonstrated. However, the mechanisms of cardiac inflammation have not been fully documented in high-fructose diet. This study shows that there are significantly increased in cardiomyocytes size and relative wall thickness of LV in high-fructose fed adult mice. With echocardiographic analysis of cardiac function, the ejection fraction (EF%) and fractional shortening (FS%) are significantly reduced at 12 weeks after 60% high-fructose diet. The mRNA and protein levels of MCP-1 are notably increased in high-fructose treated HL-1 and primary cardiomyocyte respectively. Also, the increased protein level of MCP-1 has been detected in vivo mouse model after 12 weeks feeding, resulting in the production of pro-inflammatory makers, pro-fibrotic genes expression, and macrophage infiltration. These data demonstrate that high-fructose intake induces cardiac inflammation via macrophage recruitment in cardiomyocyte, which contributes to impair cardiac function.
