谷氨酸受体对胰岛素释放和糖尿病神经病变的影响
Enza Palazzo1, Ida Marabese1, Federica Ricciardi1
1Department of Experimental Medicine, Pharmacology Division, University of Campania "L. Vanvitelli", via Costantinopoli 16, 80138 Naples, Italy.
Pharmacology & therapeutics
|September 19, 2024
概括
糖尿病神经病变与谷氨酸酸的活性有关. 向甲基酸盐受体 (mGluRs) 提供了一种治疗策略,通过调节神经传递来管理这种情况.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 药理学 药理学是指药理学的学科.
背景情况:
- 糖尿病是导致大血管和小血管并发症的主要原因,包括外围神经病变.
- 谷氨酸在胰腺β细胞的胰岛素分泌中起着至关重要的作用,并与由于中枢神经系统过活性的糖尿病神经病变的发病有关.
- 甲基酸盐受体 (mGluRs) 为调节酸盐活性提供了潜在的治疗点.
研究的目的:
- 审查谷氨酸受体在胰岛素释放和糖尿病神经病变中的作用.
- 为了探索操纵元类谷氨酸受体 (mGluRs) 治疗糖尿病神经病变的治疗潜力.
- 强调在糖尿病神经病变中对抗谷氨酸激素过活性的策略.
主要方法:
- 审查关于谷氨酸受体,胰岛素分泌和糖尿病神经病变的现有文献.
- 分类和功能的分析 甲基酸盐受体 (mGluRs) 的分类和功能 (I-III组).
- 讨论针对治疗干预的mGluRs的药理学策略.
主要成果:
- 谷氨酸信号传递是胰岛素分泌和糖尿病神经病变的组成部分.
- 代代类谷氨酸受体 (mGluRs) 提供了一种微调神经传递的手段,与离子类受体不同.
- 针对特定的mGluR群体 (激活II/III组或抑制I组) 在治疗糖尿病神经病变方面显示出有前途.
结论:
- 通过代代类谷氨酸受体 (mGluRs) 调节谷氨酸性神经传递是一种可行的糖尿病神经病变治疗方法.
- 了解谷氨酸受体的复杂作用是开发糖尿病相关并发症有效治疗的关键.
- 对mGluRs的药理向是一种有前途的策略,可以减轻糖尿病神经病变中谷氨酸激素过活的有害影响.
相关概念视频
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
1.2K
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.
Insulin and C-peptide are...
Insulin and C-peptide are...
1.2K
Hormones Regulating Blood Glucose
3.1K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
3.1K
Insulin: The Receptor and Signaling Pathways
1.2K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.2K
Glucagon-like Receptor Agonists
305
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
305
Insulin Secretory Vesicles
4.8K
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
4.8K
Oral Hypoglycemic Agents: Biguanides and Glitazones
182
Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
182


