Período peripuberal como janela ontogenética: efeitos metabólicos a longo prazo das dietas hiperlipídica e hiperglicídica em camundongos

Abstract

The peripubertal period is a pivotal ontogenetic window for the development of deleterious metabolic conditions in adulthood. Given the increasing incidence of the obese phenotype in children and adolescents worldwide, there is still a gap regarding puberty as an ontogenetic window for the development of diseases during aging. The aim of this study was to investigate the long-term metabolic effects of high-fat and high-sugar diets in mice, ingested during the peripubertal period. C57BL-6 mice were distributed into four groups: control (CO), high-fat diet (HF), high-sugar diet (HS) and a combination of both (HSHF). The animals were fed with their respective diets from 30 to 60 days. Samples and behavioral tests were carried out at 60 and 180 days of age and the insulin tolerance test (ITT) only at 180 days. The main findings of this study were that, at 60 days of age, male HSHF animals spent less time in the periphery and more time in the center of the open field, while females showed no significant differences. None of the groups of males or females showed statistical increase in body weight, retroperitoneal adipose tissue (TARP) or perigonadal adipose tissue (TAPG) at 60 days. However, there was a decrease in brown adipose tissue (TAM) in HS, HF and HSHF females. Liver weight also remained unchanged in both males and females. At 180 days, there were no significant differences in behavioral analysis in either sex. Similarly, there were no differences in body weight or TARP. However, only HSHF males showed an increase in TAPG and TAM and lower liver weight. The females showed no changes in fat weight, with lower liver weight in the HF and HSHF groups. However, only HF females showed insulin resistance during ITT. Based on these data, it was observed that dietary changes in puberty promote metabolic changes in adulthood; however, it is still necessary to study signaling pathways that may be altered in obesity.