Irregular meal habits, smoking and low education were associated with the under-report of EI. Both FR and 24hR are subjected to bias suggesting the need of refining the procedures applied in dietary assessment methods.

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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, PPARγ 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.

Mitochondria are central coordinators of energy metabolism, and changes of their physiology have long been associated with metabolic disorders. Thus, observations of energy dynamics in different cell types are of utmost importance. Therefore, tools with quick and easy handling are needed for consistent evaluations of such interventions. In this paper, our main hypothesis is that during different nutritional situations lymphocytes mitochondrial physiology could be associated with the metabolism of other cell types, such as cardiomyocytes, and consequently be used as metabolic biomarker. Blood lymphocytes and heart muscle fibers were obtained from both fed and 24 h-fasted mice, and mitochondrial analysis was assessed by high-resolution respirometry and western blotting. Carbohydrate-linked oxidation and fatty acid oxidation were significantly higher after fasting. Carnitine palmitoil transferase 1 and uncouple protein 2 contents were increased in the fasted group, while the glucose transporters 1 and 4 and the ratio phosphorylated AMP-activated protein kinase/AMPK did not change between groups. In summary, under a nutritional status modification, mitochondria demonstrated earlier adaptive capacity than other metabolic sensors such as glucose transporters and AMPK, suggesting the accuracy of mitochondria physiology of lymphocytes as biomarker for metabolic changes.