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Войти в исследования American journal of hypertension · 2026
Sucrose induces Cardiac Hypertrophy and Renal Perivascular Fibrosis in a Novel Mouse Model of Hypertension.
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Terada Yuka, Nakayama Yuki, Zhang Youjie, Cetinkaya-Un Busra, Elliott Katherine J, Hashimoto Tomoki, Adebiyi Adebowale, Osei-Owusu Patrick, Eguchi Satoru
Аннотация
BACKGROUND: Excess sugar consumption increases the risk for hypertension. We previously reported pilot data demonstrating that male mice drinking 2% sucrose water develop hypertension. However, the sucrose effects on left ventricular hypertrophy, kidney fibrosis, or sex difference in hypertension remain unclear. In the present study, we characterized the cardiac and renal pathology in a larger cohort including female mice to establish a novel sucrose-induced mouse model of hypertension associated with cardiovascular remodeling.
METHODS: Eight- to nine- week-old C57BL6 mice were given drinking water containing 2% sucrose or regular water for 4 weeks. Blood pressure was monitored using a tail-cuff system. Echocardiography was performed to evaluate cardiac remodeling. Sirius red staining was performed to evaluate heart and kidney fibrosis.
RESULTS: Male mice drinking the sucrose water developed hypertension (systolic blood pressure 122.0±1.3mmHGvs 162.2±4.3 mmHG at day 28). Sucrose treatment increased left ventricular wall thickness and induced perivascular fibrosis of the heart and kidney compared to control mice. Cardiac functions were preserved. In female mice, sucrose treatment induced milder hypertension than male mice (126.9±2.4 mmHg vs 143.7±3.2 mmHg at day 28). However, sucrose treatment caused similar degree of left ventricular hypertrophy in female mice.
CONCLUSION: Sucrose water induced hypertension, cardiac hypertrophy, and fibrosis of the heart and kidney in male mice. Female mice were partially protected from hypertension but not from cardiac hypertrophy. This mouse model represents a useful tool to investigate molecular mechanisms by which hypertension and end organ damage develop with excess sugar consumption.
METHODS: Eight- to nine- week-old C57BL6 mice were given drinking water containing 2% sucrose or regular water for 4 weeks. Blood pressure was monitored using a tail-cuff system. Echocardiography was performed to evaluate cardiac remodeling. Sirius red staining was performed to evaluate heart and kidney fibrosis.
RESULTS: Male mice drinking the sucrose water developed hypertension (systolic blood pressure 122.0±1.3mmHGvs 162.2±4.3 mmHG at day 28). Sucrose treatment increased left ventricular wall thickness and induced perivascular fibrosis of the heart and kidney compared to control mice. Cardiac functions were preserved. In female mice, sucrose treatment induced milder hypertension than male mice (126.9±2.4 mmHg vs 143.7±3.2 mmHg at day 28). However, sucrose treatment caused similar degree of left ventricular hypertrophy in female mice.
CONCLUSION: Sucrose water induced hypertension, cardiac hypertrophy, and fibrosis of the heart and kidney in male mice. Female mice were partially protected from hypertension but not from cardiac hypertrophy. This mouse model represents a useful tool to investigate molecular mechanisms by which hypertension and end organ damage develop with excess sugar consumption.