Excess of methyl donor in the perinatal period reduces postnatal leptin secretion in rat and interacts with the effect of protein content in diet

PLoS One. 2013 Jul 1;8(7):e68268. doi: 10.1371/journal.pone.0068268. Print 2013.

Abstract

Methionine, folic acid, betaine and choline interact in the one-carbon metabolism which provides methyl groups for methylation reactions. An optimal intake of these nutrients during pregnancy is required for successful completion of fetal development and evidence is growing that they could be involved in metabolic long-term programming. However, the biological pathways involved in the action of these nutrients are still poorly known. This study investigated the interaction between methyl donors and protein content in maternal diet during the preconceptual, pregnancy and lactation periods and the consequences on the rat offspring in the short and long term. Methyl donor supplementation reduced leptin secretion in offspring, whereas insulin levels were mostly affected by protein restriction. The joint effect of protein restriction and methyl donor excess strongly impaired postnatal growth in both gender and long term weight gain in male offspring only, without affecting food intake. In addition, rats born from protein restricted and methyl donor supplemented dams gained less weight when fed a hypercaloric diet. Methylation of the leptin gene promoter in adipose tissue was increased in methyl donor supplemented groups but not affected by protein restriction only. These results suggest that maternal methyl donor supplementation may influence energy homeostasis in a gender-dependent manner, without affecting food intake. Moreover, we showed that macronutrients and micronutrients in maternal diet interact to influence the programming of the offspring.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Body Weight
  • DNA Methylation
  • Diet
  • Dietary Proteins / metabolism*
  • Dietary Supplements* / analysis
  • Eating
  • Female
  • Gene Expression Regulation, Developmental
  • Lactation
  • Leptin / blood
  • Leptin / genetics
  • Leptin / metabolism*
  • Litter Size
  • Male
  • Molecular Sequence Data
  • Promoter Regions, Genetic
  • Rats / physiology*
  • Rats, Sprague-Dawley

Substances

  • Dietary Proteins
  • Leptin

Grants and funding

FG was supported by a grant from INRA and Région Pays de la Loire. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.