Abstract FR511: Sucrose elevates blood pressure in mice: a new metabolic model for human hypertension?

Introduction: 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. There are many cohort studies demonstrating a positive relationship between sweetened beverage consumption and development of hypertension. However, it remains unclear whether sucrose directly regulates blood pressure in mice. Hypothesis: Sucrose increases blood pressure and potentially causes hypertension in mice. Methods: 8~9 weeks old male C57BL6 mice were given 2% sucrose in drinking water. Fresh 2% sucrose drinking water was provided every week. Blood pressure was monitored over 4 weeks using a tail-cuff (CODA Noninvasive Blood Pressure System) and the mice were sacrificed at 4 weeks. The data were compared with no treatment mice and mice with angiotensin II (1000 ng/kg/min) infusion for 4 weeks. Results: Systolic blood pressure in mice drinking 2% sucrose water was significantly higher than untreated control mice starting at day 3 and continuing until mice were sacrificed on day 28 (mean systolic blood pressure 157.8±5.0 vs 122.2±3.0 mmHg, day28 p<0.01). Systolic blood pressure in the angiotensin II treated mice also increased starting as day 3 through day 28 (mean systolic blood pressure 177.4±3.6 mmHg at day28). The increase in systolic blood pressure in sucrose treated mice was similar to the increase in the AngII treated mice, until day 14 where the angiotensin II treatment increased systolic blood pressure more than sucrose. Sucrose treatment increased left ventricular mass compared to untreated control mice (116.5±0.66 vs 102.9±0.78 mm3, day28 p<0.05), however, the response to sucrose was not as robust as that elicited by angiotensin II. Sucrose treatment increased fibrotic area around coronary arteries over untreated control mice, which was similar to the response seen in angiotensin II treated mice. Water intake was higher in the sucrose and angiotensin II groups than in the control group (0.221 and 0.209 vs 0.148 ml/mg/day). Average sucrose consumed was 4.42 g/kg/day. There was no significant difference in body weight or blood glucose levels among the 3 groups. However, there was a tendency for higher serum insulin levels in the sucrose group Conclusions: Sucrose caused hypertension, cardiac hypertrophy and cardiac fibrosis in mice comparable to the angiotensin II model. Further investigation is necessary to explore potential mechanisms by which sucrose elevates blood pressure in mice.