Swimming training mitigates the sex‐specific hepatic disruption caused by a high‐calorie diet: The putative modulation of Nrf2/Keap‐1 pathway in male mice

Abstract

This study investigated whether swimming protocol induces adaptations to sex‐specific oxidative stress and Nrf2/Keap‐1 pathway in the liver of mice fed a high‐calorie diet (HCD) during the early life period. Male and female Swiss mice were fed a standard or high‐calorie (enriched with 20% lard and 20% corn syrup) diets, and the trained mice were subjected to a swimming protocol (5 days/week) from 21st to 49th postnatal days. Males fed a HCD had more pronounced alterations in all parameters evaluated than females. Although there was no increase in body weight, the fat deposition was higher in male mice exposed to diet. The intake of HCD induced dyslipidemia mainly in males. In a sex‐dependent manner, the hepatic markers of oxidative damage, antioxidant defences, and a sensitive sulfhydryl protein were altered in mice fed a HCD. Swimming counteracted dyslipidemia, hepatic oxidative stress, and the Nrf2/Keap‐1 signalling downregulation, in a sex‐dependent manner, in mice exposed to a HCD. These findings demonstrate that a non‐pharmacological therapy, swimming protocol, contributed to adaptations of sex‐specific hepatic oxidative stress and Nrf2/Keap‐1 regulation in male mice fed a HCD.