Abstract

The nutritional transition that the western population has undergone is increasingly associated with chronic metabolic diseases. In this work, we evaluated a diet rich in saturated fatty acids (hyperlipidic, HL) after weaning of the offspring rats submitted to maternal protein restriction on the hepatic mitochondrial bioenergetics. Wistar rats were mated and during gestation and lactation, mothers received control diets (NP, normal protein content 17%) or low protein (LP, 8% protein). After weaning, rats received either NL (normolipidic) or HL (+59% SFA) diets up to 90 days of life. It was verified that all respiratory states of hepatic mitochondria showed a reduction in the LP group submitted to the post-weaning HL diet. This group also presented greater mitochondrial swelling compared to controls, potentiated after Ca2+ addition and prevented in the presence of EGTA (calcium chelator) and cyclosporin A (mitochondrial permeability transition pore inhibitor). There was also an increase in liver protein oxidation and lipid peroxidation and reduction in catalase and glutathione peroxidase activities in the LP group fed HL diet after weaning. Our data suggest that adult rats subjected to maternal protein restriction were more susceptible to hepatic mitochondrial damage caused by a diet rich in saturated fatty acids post-weaning.

Highlights

  • According to the World Health Organization, thousands of people, mostly children, die annually or present a delay in physiological development due to nutritional deficiencies and changes in the perinatal environment

  • The body weight at 90 days was reduced in low protein (LP)-NL and LP-hyperlipidic diets (HL) when compared to NP-NL

  • In the resting condition, there was an increase in LP-NL (+63.1%, p < 0.01) and NP-HL (+75.1%, p < 0.001) compared to respective control group (NP-NL); and a decrease in LP-HL when compared with LP-NL (−32.1%, p < 0.05) and NP-HL groups (−36.8%, p < 0.01)

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Summary

Introduction

According to the World Health Organization, thousands of people, mostly children, die annually or present a delay in physiological development due to nutritional deficiencies and changes in the perinatal environment (during gestation and lactation). The underlying mechanisms are based on “phenotypic plasticity” [5,6]. A new nutritional paradigm has been configured, in which undernutrition has been replaced by overnutrition, characterizing a nutritional transition [8]. This favorable situation for the early onset of chronic-metabolic diseases is strongly associated with the consumption of hypercaloric/hyperlipidic diets [9,10], mainly westernized diets enriched in saturated fatty acids (SFA). The nutritional transition and the inversion of dietary patterns are noteworthy, where there is a high prevalence of excessive food consumption with higher palatability, such as those rich in fats and sugars [11] leading to greater prevalence of overweight and obesity

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