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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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  1. 首页
  2. 通过葡萄糖皮质激素受体增加肝脏含有黄素的单氧酶3的升高有助于妊娠糖尿病
  1. 首页
  2. 通过葡萄糖皮质激素受体增加肝脏含有黄素的单氧酶3的升高有助于妊娠糖尿病

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Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
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通过葡萄糖皮质激素受体增加肝脏含有黄素的单氧酶3的升高有助于妊娠糖尿病

Binxin Chen1, Mingyang Chen2, Xiaoyi Pan3

  • 1School of Medicine, Zhejiang University, Women's hospital, Hangzhou, China; Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, School of Medicine, Zhejiang University, Hangzhou First People's Hospital, Hangzhou, China.

Drug metabolism and disposition: the biological fate of chemicals
|September 4, 2025

在PubMed 上查看摘要

概括
此摘要是机器生成的。

妊娠诱导的皮质醇激活了肝脏含有黄素的单氧酶3 (FMO3),使妊娠糖尿病 (GDM) 的高血糖恶化. 在小鼠中,用3,3'-二醇甲抑制FMO3提高了葡萄糖耐受性.

关键词:
含有黄素的单氧酶3孕期糖尿病葡萄糖皮质类药物

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科学领域:

  • 内分泌学和新陈代谢
  • 分子生物学
  • 药理学

背景情况:

  • 孕期糖尿病 (GDM) 增加了妊娠并发症和终身代谢障碍的风险.
  • 皮质醇和肝脏含有黄素单氧酶3 (FMO3) 的升高与GDM有关,但它们的相互作用尚不清楚.

研究的目的:

  • 阐明皮质醇影响GDM中的FMO3的机制.
  • 研究皮质醇-FMO3轴在GDM病变中的作用.
  • 评估FMO3抑制作为GDM的治疗策略.

主要方法:

  • 研究了涉及皮质醇,葡萄糖皮质体受体和肝脏FMO3的信号通路.
  • 评估了FMO3对三甲基胺N氧化物 (TMAO) 生产和高血糖的影响.
  • 在GDM小鼠模型中利用了FMO3的药理抑制.

主要成果:

  • 在GDM中皮质醇的升高激活了葡萄糖皮质体受体,提高了肝脏FMO3的调节.
  • 上调的FMO3增加了肝脏TMAO的产生,通过Akt-FOXO1-G6PC轴加剧了高血糖.
  • 通过降低TMAO和抑制Akt-FOXO1-G6PC通路,使用3,3'- diindolylmethane抑制FMO3改善了孕期小鼠的葡萄糖耐受性.

结论:

  • 在GDM中确定了一种新的葡萄皮质激素驱动的肝脏FMO3调节机制.
  • 在GDM中,FMO3是高血糖的关键媒介.
  • 3,3' - - 迪因多利甲具有改善GDM葡萄糖平衡的治疗作用.