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由高脂肪饮食诱导的代际遗传导致高和下丘脑对胰岛素和瘦素的敏感性降低在第二代大鼠中
Rosana da Conceição Araújo Maia1, Taynara Carolina Lima1, Claudiane Maria Barbosa1
1Núcleo de Pesquisa em Ciências Biológicas, Programa de Pós-Graduação em Ciências Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, Brazil.
Nutrition (Burbank, Los Angeles County, Calif.)
|January 25, 2024
概括
祖先大鼠的高脂肪饮食诱导了后代的代际变化,导致增加食物摄入量,胰岛素耐药性和肥胖. 这些效应表明,父母的饮食与后代的心脏代谢健康之间存在联系.
科学领域:
- 代谢障碍 代谢障碍 代谢障碍
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 神经内分泌学神经内分泌学
背景情况:
- 母亲高脂肪饮食 (HFD) 与不良后代健康结果有关.
- 对于HFD对代谢调节的代际影响需要进一步研究.
- 控制腹感的脑下垂体通路对于能量平衡至关重要.
研究的目的:
- 为了研究HFD对胰岛素和瘦素敏感性的代际影响,在腹的下丘脑控制中.
- 为了评估第二代后代对这些影响的评估,后代被食控制饮食.
主要方法:
- 原始老鼠被食HFD或控制饮食;后代 (F1和F2) 被食控制饮食.
- 评估的体质,脂肪指数和与胰岛素/素信号传递和腹神经相关的下丘脑基因表达.
- 评估了DNA甲基转移酶3a,ACE2,AT2R,胰岛素/瘦素路径组件,SOD活性和碳基蛋白度.
主要成果:
- HFD原始体表现出胰岛素耐药性和降低β细胞功能.
- 来自HFD祖先的第二代后代表现出增加的食物摄入量,胰岛素耐药性,体重和脂肪.
- 脑下垂体的变化包括DNMT3a,AgRP,AT1R和NADPH氧化酶的增加,胰岛素/叶丁信号元件和POMC的减少.
结论:
- 父母HFD通过表观遗传机制诱导下丘脑和控制的代际变化.
- 这些变化促进了后代的多,胰岛素抵抗和肥胖,增加了心脏代谢疾病的风险.
- 代谢功能障碍的代际遗传突出了父母饮食对后代健康的影响.
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