title: Global DNA methylation was changed by a maternal high-lipid, high-energy diet during gestation and lactation in male adult mice liver.
abstract: An epigenetic mechanism has been suggested to explain the effects of the maternal diet on the development of disease in offspring. The present study aimed to observe the effects of a maternal high-lipid, high-energy (HLE) diet on the DNA methylation pattern of male offspring in mice. Female C57BL/6J mice were fed an HLE diet during gestation and lactation. The genomic DNA methylations at promoter sites of genes in the liver, mRNA and protein levels of selected genes related to lipid and glucose metabolism were measured by microarray, real-time PCR and Western blot. The results indicated that the percentage of methylated DNA in offspring from dams that were fed an HLE diet was significantly higher than that from dams that were fed a chow diet, and most of these genes were hypermethylated in promoter regions. The nuclear protein content and mRNA levels of hypermethylated genes, such as PPARγ and liver X receptor α (LXRα), were decreased significantly in offspring in the HLE group. The results suggested that the DNA methylation profile in adult offspring livers was changed by the maternal HLE diet during gestation and lactation.
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Huan-Ling
authors.initials: HL
authors.lastname: Yu
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Shan
authors.initials: S
authors.lastname: Dong
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Li-Fang
authors.initials: LF
authors.lastname: Gao
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Yuan-Di
authors.initials: YD
authors.lastname: Xi
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Wei-Wei
authors.initials: WW
authors.lastname: Ma
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Lin-Hong
authors.initials: LH
authors.lastname: Yuan
authors.affiliation: School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University,Beijing100069,People's Republic of China.
authors.forename: Rong
authors.initials: R
authors.lastname: Xiao
mesh_terms: D000818:Animals; D019175:DNA Methylation; D059305:Diet, High-Fat / Q000009:adverse effects*; D002149:Energy Intake; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development; D018507:Gene Expression Regulation, Developmental; D007774:Lactation; D008099:Liver / Q000254:growth & development / Q000378:metabolism*; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D008810:Mice, Inbred C57BL; D011247:Pregnancy; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms; D015854:Up-Regulation; D014886:Weaning
chemical_list: D012333:RNA, Messenger
keywords: Epigenetic mechanisms