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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.

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相关实验视频

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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
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内皮胰岛素抵抗恶化 实验性牙周炎

T Zeze1, T Shinjo1, K Sato1

  • 1Section of Periodontology, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.

Journal of dental research
|July 14, 2023
PubMed
概括

牙内皮胰岛素抵抗通过增加VCAM1表达和白细胞粘附来促进牙周炎. 这通过减少PI3K/Akt/FoxO1通路激活而发生,恶化气泡骨损失.

关键词:
这是一个VCAM-1系统.气泡骨损失是指气泡骨损失的发生.细胞粘附分子的细胞粘附分子甲盒蛋白质O1 是一种甲盒蛋白质.牙周疾病 牙周疾病2 型糖尿病 2 型糖尿病

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科学领域:

  • 口腔生物学 口腔生物学
  • 内分泌学 在内分泌学.
  • 免疫学 免疫学 免疫学

背景情况:

  • 在糖尿病患者中,牙周炎的严重程度更高.
  • 与糖尿病相关的牙周炎的分子机制尚不清楚.
  • 牙组织中的胰岛素抵抗可能会导致糖尿病并发症.

研究的目的:

  • 调查牙周炎病原发生过程中牙的作用中的内皮胰岛素耐药性.
  • 阐明将内皮胰岛素抵抗与牙周炎联系起来的分子机制.

主要方法:

  • 通过PI3K/Akt途径检查了胰岛素对内皮细胞 (ECs) 中VCAM1表达的作用.
  • 使用了血管内皮细胞特异性胰岛素受体淘汰 (VEIRKO) 的小鼠.
  • 分析了FoxO1在胰岛素介导的VCAM1调节和白细胞粘附中的作用.

主要成果:

  • 胰岛素治疗通过PI3K/Akt降低了EC中的VCAM1表达,减少了白细胞粘附.
  • 超血糖引起的胰岛素抵抗在ECs减少了胰岛素对VCAM1.1的影响.
  • 在VEIRKO小鼠中,牙周炎和骨质损失增加,VCAM1,TNFα,MCP-1和RANKL的上调.
  • 在VEIRKO小鼠和经过高血糖治疗的EC中,胰岛素介导的FoxO1激活被抑制.
  • 突变的FoxO1减弱了胰岛素对VCAM1和白细胞粘附的调节.

结论:

  • 内皮胰岛素抵抗有助于牙周炎的进展.
  • 失调的VCAM1表达和白细胞粘附是PI3K/Akt/FoxO1信号受损的结果.
  • 向内皮胰岛素抵抗可能为糖尿病患者的牙周炎提供治疗策略.