title: The influence of a high-fat dietary environment in the fetal period on postnatal metabolic and immune function.
abstract: Few reports show whether a high-fat (HF) dietary environment in the fetal period affects immune function or the development of lifestyle-related disease at maturity. We examined the influence of an HF dietary environment in the fetal period on postnatal metabolic and immune function. A total of 16 pregnant mice were given control (CON) diet and 16 were given HF diet in the gestational period, from mating to delivery. After delivery lactating mice were given either CON or HF diet, resulting in four groups. After weaning, the offspring mice were given the same diet that their mothers received during lactation. HF dietary intake in the postnatal period increased fat pad weights, serum glucose, and leptin levels. An HF diet in the fetal period resulted in fewer splenic lymphocytes, a thinner thymic cortex, and impaired antigen-specific immune reactions. Furthermore, tumor necrosis factor (TNF)-alpha production and serum triglyceride levels were elevated in the fetal HF group. In addition, the HF-HF group showed a consistent decrease in ovalbumin (OVA)-specific IgG and elevation of IgE, associated with advanced fatty changes in the liver. Results from this study suggest that HF environment during the fetal period induces epigenetic propensity toward obesity and immunological burden in part due to increased adipose tissue mass, significant reduction in the number of immune cells and decreased activities of immune cells.
authors.affiliation: Department of Food and Nutrition, Japan Women's University, Tokyo, Japan.
authors.forename: Yukino
authors.initials: Y
authors.lastname: Odaka
authors.forename: Mana
authors.initials: M
authors.lastname: Nakano
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tanaka
authors.forename: Tomoko
authors.initials: T
authors.lastname: Kaburagi
authors.forename: Haruka
authors.initials: H
authors.lastname: Yoshino
authors.forename: Natsuko
authors.initials: N
authors.lastname: Sato-Mito
authors.forename: Kazuto
authors.initials: K
authors.lastname: Sato
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004041:Dietary Fats / Q000494:pharmacology*; D004777:Environment; D044127:Epigenesis, Genetic; D005234:Fatty Liver / Q000209:etiology / Q000473:pathology; D005260:Female; D007109:Immunity / Q000187:drug effects*; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D020738:Leptin / Q000097:blood; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000276:immunology; D013154:Spleen / Q000276:immunology / Q000473:pathology; D013950:Thymus Gland / Q000473:pathology; D014280:Triglycerides / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D007074:Immunoglobulin G; D020738:Leptin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D007073:Immunoglobulin E; D010047:Ovalbumin