title: Maternal methyl donors supplementation during lactation prevents the hyperhomocysteinemia induced by a high-fat-sucrose intake by dams.
abstract: Maternal perinatal nutrition may program offspring metabolic features. Epigenetic regulation is one of the candidate mechanisms that may be affected by maternal dietary methyl donors intake as potential controllers of plasma homocysteine levels. Thirty-two Wistar pregnant rats were randomly assigned into four dietary groups during lactation: control, control supplemented with methyl donors, high-fat-sucrose and high-fat-sucrose supplemented with methyl donors. Physiological outcomes in the offspring were measured, including hepatic mRNA expression and global DNA methylation after weaning. The newborns whose mothers were fed the obesogenic diet were heavier longer and with a higher adiposity and intrahepatic fat content. Interestingly, increased levels of plasma homocysteine induced by the maternal high-fat-sucrose dietary intake were prevented in both sexes by maternal methyl donors supplementation. Total hepatic DNA methylation decreased in females due to maternal methyl donors administration, while Dnmt3a hepatic mRNA levels decreased accompanying the high-fat-sucrose consumption. Furthermore, a negative association between Dnmt3a liver mRNA levels and plasma homocysteine concentrations was found. Maternal high-fat-sucrose diet during lactation could program offspring obesity features, while methyl donors supplementation prevented the onset of high hyperhomocysteinemia. Maternal dietary intake also affected hepatic DNA methylation metabolism, which could be linked with the regulation of the methionine-homocysteine cycle.
authors.forename: Paul
authors.initials: P
authors.lastname: Cordero
authors.forename: Fermin I
authors.initials: FI
authors.lastname: Milagro
authors.forename: Javier
authors.initials: J
authors.lastname: Campion
authors.affiliation: Department of Nutrition, Food Science and Physiology, University of Navarra, 31008 Pamplona, Spain. jalfmtz@unav.es.
authors.forename: J Alfredo
authors.initials: JA
authors.lastname: Martinez
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004248:DNA (Cytosine-5-)-Methyltransferases / Q000235:genetics / Q000378:metabolism; D019175:DNA Methylation / Q000187:drug effects; D000090205:DNA Methyltransferase 3A; D059305:Diet, High-Fat; D019422:Dietary Sucrose; D019587:Dietary Supplements; D005260:Female; D006710:Homocysteine / Q000097:blood; D020138:Hyperhomocysteinemia / Q000517:prevention & control*; D007774:Lactation; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena / Q000187:drug effects; D009765:Obesity / Q000517:prevention & control; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012436:S-Adenosylmethionine / Q000494:pharmacology
chemical_list: D019422:Dietary Sucrose; D012333:RNA, Messenger; D006710:Homocysteine; D012436:S-Adenosylmethionine; D004248:DNA (Cytosine-5-)-Methyltransferases; D000090205:DNA Methyltransferase 3A