孕期孕产妇肥胖性饮食及其对子肝功能的影响
Ashley S Meakin1, Peter W Nathanielsz2, Cun Li2
1Early Origins of Adult Health Research Group, Health and Biomedical Innovation, Clinical & Health Sciences, University of South Australia, Adelaide, Australia.
Obesity (Silver Spring, Md.)
|August 30, 2024
概括
的孕产妇肥胖会降低肝脏酶的活性,特别是在雄性动物中,这是由于葡萄糖皮质醇受体信号的改变造成的. 这突显了晚年性特定肝病风险的潜在机制.
科学领域:
- 生殖生物学和毒理学.
- 内分泌学和代谢性疾病.
- 肝病学和肝脏疾病.
背景情况:
- 孕产妇肥胖 (MO) 与后代晚年患肝病的风险增加有关,特别是在男性中.
- 这种风险可能源于细胞染色体P450 (CYP) 酶活性受损,受胎儿发育期间荷尔蒙变化的影响.
- 葡萄糖皮质体受体 (GR) 信号传导,对于调节CYP活性至关重要,可以通过替代GR异型表达来修改.
研究的目的:
- 调查孕产妇肥胖是否会导致GR异型表达和局部化在胎儿肝中的性别特异性变化.
- 确定这些变化是否有助于减轻肥胖母亲后代的肝脏CYP活性.
- 探索与孕产妇肥胖相关的性别特异性肝病风险的潜在机制.
主要方法:
- 在怀孕之前和怀孕期间,们被食为对照或高脂肪,高能量饮食 (HF-HED).
- 胎儿肝脏样本是在怀孕165天收集的,用于分析.
- 通过功能性测定测量CYP活性,并通过RT-PCR和西欧斑块量化GR表达 (总和异型).
主要成果:
- 在HF-HED组中,整体CYP3A活性降低了.
- 从HF-HED组的男性后代中,CYP2B6活性特别降低.
- 总GR表达在HF-HED组中升高,仅在男性中观察到对抗性GRβ异型的核表达增加.
结论:
- 肥胖母亲的男性后代中肝脏CYP活性降低可能部分是由于葡萄糖皮质激素信号受损.
- 改变GR异型表达,特别是男性的GRβ增加,似乎是关键机制.
- 这些发现确定了潜在的治疗点,以减轻与孕产妇肥胖相关的性别特异性肝病风险.
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