Impact of early postnatal overnutrition on cardiac mitochondrial dysfunction in adult mice with ischemia/reperfusion.

Background And Aims: Nutritional imbalance at the beginning of life, a critical window period, leads to the development of obesity, overweight, dyslipidemia, diabetes, and cardiovascular disease in adulthood. In this study, the effects and associations of overnutrition during lactation on energy metabolism and oxidative stress in cardiomyocytes of adult male Swiss mice were examined.

Methods And Results: Animals were divided into two groups (control and overfed) subjected to baseline and ischemia/reperfusion conditions, forming four groups: control baseline (CBL), control ischemia/reperfusion (CIR), overfed baseline (OBL), and overfed ischemia/reperfusion (OIR).

Ghrelin signaling in heart remodeling of adult obese mice.

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor (GHS-R), has been suggested to be associated to obesity, insulin secretion, cardiovascular growth and homeostasis. GHS-R has been found in most of the tissues, and among the hormone action it is included the regulation of heart energy metabolism. Therefore, hypernutrition during early life leads to obesity, induces cardiac hypertrophy, compromises myocardial function, inducing heart failure in adulthood.

Early life overfeeding decreases acylated ghrelin circulating levels and upregulates GHSR1a signaling pathway in white adipose tissue of obese young mice.

Ghrelin is a hormone synthesized by the stomach that acts in different tissues via a specific receptor (GHS-R1a), including hypothalamus and adipose tissue. For instance, recent reports have shown that ghrelin has a direct action on hypothalamic regulation of food intake mainly inducing an orexigenic effect. On the other hand, ghrelin also modulates energy stores and expenditure in the adipocytes.