title: The combination of maternal and offspring high-fat diets causes marked oxidative stress and development of metabolic syndrome in mouse offspring.
abstract: Maternal overnutrition (e.g., high-fat (HF) diet) during pregnancy and lactation is believed to cause oxidative stress and increase the risk of metabolic syndrome in offspring. In the present study, we investigated the effects of both maternal and offspring HF diets on metabolic syndrome risk and oxidative stress profiles in mice. Dams of the C57BL/6J mouse strain were fed a HF or control (CO) diet during gestation and lactation. Offspring were weaned at 3weeks of age. The female offspring were sacrificed at weaning, while the males were maintained on the HF or CO diet until 11weeks of age. Tissue samples, including those from liver, were collected from offspring at 3 and 11weeks of age, and lipids, phosphatidylcholine hydroperoxide (PCOOH, an oxidative stress marker), and gene expression were evaluated. Accumulation of lipids, but not PCOOH, was found in the livers of 3-week-old offspring from dams fed the HF diet. When the offspring were maintained on a HF diet until 11weeks of age, marked accumulation of both liver lipids and PCOOH was observed. PCOOH manifestation was supported by the expression of genes such as Gpx4, encoding a PCOOH degrading enzyme. These results suggest that the combination of maternal and offspring overnutrition causes marked oxidative stress in offspring, which accelerates metabolic syndrome. The present findings in offspring from infancy to adulthood may be useful for better understanding the cause-and-effect relationships between oxidative stress and metabolic syndrome development.
authors.affiliation: Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
authors.forename: Junya
authors.initials: J
authors.lastname: Ito
authors.affiliation: Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan. Electronic address: nkgw@m.tohoku.ac.jp.
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Nakagawa
authors.affiliation: Division of Endocrinology and Metabolism, Department of Medicine, Nippon Medical School, Tokyo 113-8603, Japan.
authors.forename: Shunji
authors.initials: S
authors.lastname: Kato
authors.affiliation: Vascular Biology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.
authors.forename: Taiki
authors.initials: T
authors.lastname: Miyazawa
authors.affiliation: Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
authors.forename: Fumiko
authors.initials: F
authors.lastname: Kimura
authors.affiliation: Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
authors.forename: Teruo
authors.initials: T
authors.lastname: Miyazawa
mesh_terms: D000818:Animals; D059305:Diet, High-Fat / Q000009:adverse effects*; D005260:Female; D047109:Fetal Development; D015870:Gene Expression / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000209:etiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D044343:Overnutrition / Q000150:complications; D018384:Oxidative Stress; D010713:Phosphatidylcholines / Q000097:blood; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
chemical_list: D008055:Lipids; D010713:Phosphatidylcholines; C057590:phosphatidylcholine hydroperoxide; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase; C000611332:glutathione peroxidase 4, mouse
keywords: Fetal programming model; Gpx4; Metabolic syndrome; Oxidative stress; PCOOH