A new mouse model of hypertension using sucrose

Sucrose is a disaccharide composed of glucose and fructose linked by an α-1,2-glycosidic bond. It is a major sweetener and the main ingredient in table sugar. Although there are many cohort studies in humans that have reported the positive relationship between the consumption of sweetened beverages and the development of hypertension, there are a few reports regarding sucrose specific effects on human blood pressure. In a study of a female cohort followed from pregnancy to 10 years after childbirth, the consumption of sucrose was shown to be an independent risk factor for the development of hypertension. In rats, it has been reported that chronic sucrose intake (20% in drinking water) increased blood pressure from 102 mmHg to 129 mmHg. As long as we surveyed, however, there is no report available that examined the effects of sucrose on blood pressure in mice. Here we tested our hypothesis that sucrose increases blood pressure and potentially causes hypertension in C57BL6J mice. 8-9 week old male C57BL6 mice were given 2% sucrose in drinking water, and the water was changed in every week. Blood pressure was monitored over 4 weeks using a tail-cuff system and other related factors were examined at 4 weeks. The data were compared with the normal water group and angiotensin II (AngII 1000 ng/kg/min)-induced hypertensive mice group. The amount of water intake was significantly higher in the sucrose and AngII group than in the normal water group (0.236 and 0.209 vs 0.138 ml/mg/day p<0.01), and the average sucrose consumed was 4.73 mg/kg/day. There was no significant difference in body weight or blood glucose levels within the 3 groups. Compared to the normal water group, sucrose significantly increased the systolic blood pressure from day 7 and it continued to be elevated until day 28 (mean systolic blood pressure 163.9±5.0 vs 122.9±3.0 mmHg, day28 p<0.01). Systolic blood pressure in the AngII group was also increased significantly increased compared to the normal drinking water group on day 3 to day 28 (mean systolic blood pressure 177.4±3.6 mmHg at day28). Elevation in blood pressure was not significantly different compared with the sucrose group from day 7 to 28. Moreover, sucrose and AngII significantly increased LV mass on echocardiography (123.5±0.66 vs 102.9±0.78 mm3, day28 p<0.01) and significantly enlarged the fibrotic area around the coronary arteries histologically (ratio 0.596±0.043 vs 0.385±0.012, day28 p<0.01) compared to the normal water group. In addition, there was a tendency for serum insulin levels to increase in the sucrose group. In conclusion, sucrose appeared to cause hypertension, cardiac hypertrophy and cardiac fibrosis comparable to AngII in mice. The potential molecular mechanism likely involves insulin resistance caused by sucrose. This new hypertension model in mice which does not require any surgery, will be useful tool to explore the molecular mechanisms and pathology of sugar-induced hypertension. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.