相关实验视频
Updated: Jun 26, 2025

06:09
An In Ovo Model for Testing Insulin-mimetic Compounds
Published on: April 23, 2018
10.6K
一种in-silico建模方法来分离外源和内源血胰岛素外观,并应用于吸入胰岛素
Agnese Piersanti1, Giovanni Pacini2, Andrea Tura3
1Department of Information Engineering, Università Politecnica Delle Marche, Via Brecce Bianche 12, Ancona, Italy.
Scientific reports
|May 13, 2024
概括
这项研究开发了一个动态模型,以区分吸入和天然胰岛素. 吸入胰岛素在食测试期间显著降低了天然胰岛素分泌.
科学领域:
- 药理动力学和药理动力学
- 在生物学中的数学建模.
- 内分泌学 在内分泌学.
背景情况:
- 精确量化胰岛素来源对于糖尿病管理至关重要.
- 区分外源性 (给予) 和内源性 (自然产生的) 胰岛素是复杂的.
- 吸入胰岛素提供了另一种输送方法,但其对内源分泌的影响需要精确评估.
研究的目的:
- 开发和验证一种动态的,基于模型的方法来分离外源和内源胰岛素对血胰岛素水平的贡献.
- 应用这种新的方法来评估吸入胰岛素在标准化食测试期间对内源性胰岛素分泌的影响.
- 为了确定吸入Technosphere®胰岛素的生物可用性.
主要方法:
- 采用了三个步骤的动态in-silico建模策略.
- 21名健康受试者参加了两个标准化食测试.
- 吸入胰岛素 (Technosphere® Insulin) 在一个测试之前进行;另一个作为对照.
主要成果:
- 该模型成功地区分了外源和内源胰岛素成分.
- 吸入胰岛素使用时观察到内源性胰岛素分泌的显著减少 (p < 0.01).
- 吸入胰岛素进入血的生物可用性约为42%±21%.
结论:
- 开发的in-silico模型有效量化了外源和内源胰岛素贡献.
- 吸入胰岛素的使用显然抑制了饮食期间内源性胰岛素的分泌.
- 这种建模方法为吸入胰岛素的药理动力学及其生理影响提供了宝贵的见解.
相关概念视频
Insulin: Biosynthesis, Chemistry, and Preparation
374
The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
374
Insulin Secretory Vesicles
4.9K
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...
4.9K
Insulin Formulations: Types and Delivery
191
Insulin preparations are categorized by their duration of action into short-acting and long-acting types. Two strategies are used to modify insulin's absorption and pharmacokinetic profile: slowing the absorption post-subcutaneous injection, or altering human insulin's amino acid sequence or protein structure. These changes retain the insulin's ability to bind to the insulin receptor, but alter its behavior in solution or after injection.
Short-acting insulins are divided into...
Short-acting insulins are divided into...
191
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
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
318
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...
318

