Maternal high-fat diet causes insulin resistance of offspring via inflammatory change in visceral fat using mice models - for a remedial strategy-

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462548
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Ehime University (2015); Tohoku University (2013)
• Principal Investigator: Sugiyama Takashi 愛媛大学, 医学(系)研究科(研究院), 教授 (10263005)
• Co-Investigator(Kenkyū-buntansha): Kimura Yoshitaka 東北大学, 医学系研究科, 教授 (40261622) ; Ihara Motomasa 東北大学, 大学病院, 助教 (50403506) ; Sugawara Junichi 東北大学, 東北メディカル・メガバンク機構, 教授 (60280880)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 妊娠 / 肥満 / インスリン抵抗性 / 炎症 / 高脂肪食 / 次世代 / 子宮内環境

Outline of Final Research Achievements

We investigated the effect of maternal obesity with or without nicotine treatment on her offspring using obesity mice model. Female 6-weeks-old mice were fed either normal chow diet (CD: 10 kcal% fat) or high-fat diet (HFD: 45 kcal% fat) for 4 weeks before mating and throughout pregnancy. Nicotine was injected into pregnant litters during mid to late pregnancy. Maternal obesity with nicotine treatment causes glucose intolerance with insulin resistance through macrophage infiltration with increased levels of inflammatory cytokines and decreased levels of adiponectin in her offspring. Also, n-3 PUFA treatment for offspring in HFD fed litter caused amelioration of insulin resistance. Thus, we suggest that this obese mice model is a useful tool to assess mechanisms of metabolic syndrome in the offspring.

Free Research Field

周産期医学、代謝・内分泌学