Effect of maternal protein restriction on liver metabolism in rat offspring

Camila Moraes1, Hércules J Rebelato, Maria Esmeria C Amaral

  • 1Biomedical Sciences Graduate Program, Centro Universitário Hermínio Ometto, Uniararas, Av Maximiliano Baruto 500, 13607-339, Araras, SP, Brazil.

Insights

Gestational protein restriction (GPR) in rats protected liver mitochondria from oxidative stress, with female offspring showing enhanced protection and phosphorylation efficiency.

Area of Science:

  • Biochemistry
  • Developmental Biology
  • Maternal-Fetal Nutrition

Background:

  • Gestational protein restriction (GPR) is a significant nutritional insult with potential long-term consequences for offspring health.
  • Maternal nutrition during pregnancy critically influences fetal development and metabolic programming.
  • Understanding the impact of GPR on liver metabolism is crucial for identifying early life interventions.

Purpose of the Study:

  • To investigate the effects of GPR on liver metabolism and mitochondrial function in 30-day-old rat offspring.
  • To determine if GPR confers protection against oxidative stress in the liver.
  • To explore potential sex-specific differences in response to GPR.

Main Methods:

  • Pregnant rats were fed either a normal protein (NP) or low-protein (LP) diet.
  • Livers and mitochondria were collected from 30-day-old offspring for biochemical analysis.
  • Mitochondrial function was assessed by measuring swelling, oxygen uptake, and ADP/O ratio.
  • Lipid peroxidation was evaluated by quantifying thiobarbituric acid reactive substances (TBARS).

Main Results:

  • LP offspring exhibited increased hepatic and muscle glycogen levels.
  • Mitochondrial swelling and oxygen consumption were reduced in NP female and LP offspring.
  • Reduced TBARS production in females indicated inhibited lipid peroxidation.
  • LP female offspring showed a higher ADP/O ratio, suggesting improved mitochondrial phosphorylation efficiency.

Conclusions:

  • GPR protects liver mitochondria against oxidative stress in early life.
  • Female rat offspring appear more resistant to the adverse effects of GPR on liver mitochondria.
  • GPR may enhance mitochondrial phosphorylation efficiency, particularly in females.

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