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. This dual action has suggested that this
hormone may act as a link between the central nervous system and peripheral mechanisms. Furthermore, concerning
nutritional disorders, it has been suggested that
obesity may be considered an impairment of the above cited link. Therefore, considering that neonatal overfeeding induces
obesity in adulthood by unknown mechanisms, in this study we examined the effects of early life
overnutrition on the development of
obesity and in particular on adipose tissue
ghrelin signaling in young mice. Our data demonstrated that
overnutrition during early life induces a significant increase in
body weight of young mice, starting
at 10 days, and this increase in weight persisted until adulthood (90 days of age). In these animals,
blood glucose, liver weight and visceral fat weight were found higher at 21 days when compared to the control group. Acylated
ghrelin circulating levels were found lower in the young obese pups. In addition, in white adipose tissue
ghrelin receptor (GHS-R1a) expression increased and was associated to positive modulation of content and phosphorylation of
proteins involved in cell energy store and use as AKT, PI3K, AMPK, GLUT-4, and CPT1. However, PPARĪ³ content decreased in obese group. Basically, we showed that adipose tissue metabolism is altered in early life acquired
obesity and probably due to such modification a new pattern of
ghrelin signaling pathway takes place.