Abstract 12767: Postnatal Overfeeding in Mice Leads to Overweight and to Cardiometabolic and Oxidative Alterations in Adulthood
Introduction: Several studies in mice have shown that postnatal overfeeding (OF) induces permanent moderate increase of body weight in the adult life; however, cardiovascular repercussions of postnatal OF are less known.
Methods: Immediately after birth, and during 3 weeks, litters of C57BL/6 mice were either maintained at 10 (normal-fed group, NF), or reduced to 3 in order to induce an OF situation. At weaning, mice of both groups received a standard diet. Measurements of phenotypic characteristics and metabolic parameters (cholesterol, insulin and leptin) were performed in the plasma at 7 months. Tissue oxidative stress was assessed by Electron Paramagnetic Resonance in the heart using CP spin probe. Cardiac function was measured by echocardiography and the susceptibility to myocardial global ischemia and reperfusion was assessed ex vivo in isolated perfused heart.
Results: OF led to an increase in body weight (+30%) as compared to NF group. Significant increases of plasma cholesterol, insulin and leptin levels were observed in OF mice as compared to NF mice. Myocardial CP radical was increased in OF mice compared to NF mice. In vivo, diastolic (97vs114 mmHg, p<0.05) and systolic (126vs140 mmHg) blood pressure were significantly higher in OF than NF mice. Moreover, LV shortening and ejection fraction were decreased in OF mice. Ex vivo, after 30 min of ischemia, hearts isolated from mice that underwent postnatal OF showed lower recovery of coronary flow (35% vs 55%, p<0.05) and developed ventricular pressure. Moreover, infarct size evaluated after 2 hours of reperfusion was increased in OF group (31%vs 54%, p<0.05) as compared to NF.
Conclusion: These results show that OF induces metabolic, oxidative and functional disturbances but also a higher susceptibility to cardiac functional damage after ischemia ex vivo. Complementary data are required to understand the cellular pathways implicated in these metabolic and cardiovascular modifications.
- © 2011 by American Heart Association, Inc.