The combination of maternal and offspring high-fat diets causes marked oxidative stress and development of metabolic syndrome in mouse offspring

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• 作者：Junya Ito^a ; Kiyotaka Nakagawa^a ; ^{nkgw@m.tohoku.ac.jp" class="auth_mail" title="E-mail the corresponding author} ; Shunji Kato^b ; Taiki Miyazawa^c ; Fumiko Kimura^a ; Teruo Miyazawa^a
• 关键词：HF ; high-fat ; CO ; control ; PCOOH ; phosphatidylcholine hydroperoxide ; Gpx1 ; glutathione peroxidase 1 ; Sod1 ; superoxide dismutase 1 ; Gpx4 ; glutathione peroxidase 4 ; Cat ; catalase ; Gclm ; glutamate-cysteine ligase modifier subunit ; PC ; phosphatidylcholine ; CL-HPLC ; chemiluminescence detection ; TBARS ; thiobarbituric acid reactive substances ; TG ; triglyceride ; TC ; total cholesterol ; PL ; phospholipid ; Aco2 ; acyl-CoA oxidase 2 ; Cpt2 ; carnitine palmitoyltransferase 2 ; Gclc ; glutamate-cysteine ligase cata
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：15 April 2016
• 年：2016
• 卷：151
• 期：Complete
• 页码：70-75
• 全文大小：770 K

文摘

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 3 weeks of age. The female offspring were sacrificed at weaning, while the males were maintained on the HF or CO diet until 11 weeks of age. Tissue samples, including those from liver, were collected from offspring at 3 and 11 weeks 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 11 weeks 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.