Short-Term Postnatal Overfeeding Induces Long-Lasting Cardiometabolic Syndrome in Mature and Old Mice Associated with Increased Sensitivity to Myocardial Infarction.

SCOPE: Perinatal nutritional disturbances may "program" an increased cardio-metabolic risk in adulthood; however, few experimental studies have explored their effects on mature and/or old animal. This study aims to investigate the influence of postnatal overfeeding (PNOF) on cardiac function, sensitivity to ischemia-reperfusion (I-R) injury in vivo, glucose metabolism, and metabolic profile of pericardial adipose tissue (PAT) in young (4 months), adult (6 months), old (12 months), and very old (18 months) male mice. METHODS AND RESULTS: Two days after birth, PNOF is induced by adjusting the litter size of C57BL/6 male mice to three pups/mother, while the normally fed (NF) control group is normalized to nine pups/mother. After weaning, all mice have free access to standard diet. Glucose/insulin tests and in vivo myocardial I-R injury are conducted on mice aged from 2 to 12 months, while echocardiography is performed at all ages up to 18 months. PNOF mice exhibit an early and persistent 10-20% increase in body weight and a 10% decrease in left ventricular ejection fraction throughout their lifespan. In PNOF mice aged 4, 6, and 12 months, glucose intolerance and insulin resistance are observed, as well as a 27-34% increase in infarct size. This is accompanied by a higher PAT mass with increased inflammatory status. CONCLUSION: Short-term PNOF results in nutritional programming, inducing long-lasting alterations in glucose metabolism and cardiac vulnerability in male mice, lasting up to 12 months.

Differential Cerebral Gustatory Responses to Sucrose, Aspartame, and Stevia Using Gustatory Evoked Potentials in Humans.

Aspartame and Stevia are widely substituted for sugar. Little is known about cerebral activation in response to low-caloric sweeteners in comparison with high-caloric sugar, whereas these molecules lead to different metabolic effects. We aimed to compare gustatory evoked potentials (GEPs) obtained in response to sucrose solution in young, healthy subjects, with GEPs obtained in response to aspartame and Stevia. Twenty healthy volunteers were randomly stimulated with three solutions of similar intensities of sweetness: Sucrose 10 g/100 mL of water, aspartame 0.05 g/100 mL, and Stevia 0.03 g/100 mL. GEPs were recorded with EEG (Electroencephalogram) electrodes. Hedonic values of each solution were evaluated using the visual analog scale (VAS). The main result was that P1 latencies of GEPs were significantly shorter when subjects were stimulated by the sucrose solution than when they were stimulated by either the aspartame or the Stevia one. P1 latencies were also significantly shorter when subjects were stimulated by the aspartame solution than the Stevia one. No significant correlation was noted between GEP parameters and hedonic values marked by VAS. Although sucrose, aspartame, and Stevia lead to the same taste perception, cerebral activation by these three sweet solutions are different according to GEPs recording. Besides differences of taste receptors and cerebral areas activated by these substances, neural plasticity, and change in synaptic connections related to sweet innate preference and sweet conditioning, could be the best hypothesis to explain the differences in cerebral gustatory processing after sucrose and sweeteners activation.