Lenbury2001_InsulinKineticsModel_A

This a model from the article:
Modeling insulin kinetics: responses to a single oral glucose administration or ambulatory-fed conditions.

Lenbury Y, Ruktamatakul S, Amornsamarnkul S. Biosystems.
2001 Jan;59(1):15-25. 11226623
,
Abstract:

This paper presents a nonlinear mathematical model of the glucose-insulin feedback system, which has been extended to incorporate the beta-cells' function on maintaining and regulating plasma insulin level in man. Initially, a gastrointestinal absorption term for glucose is utilized to effect the glucose absorption by the intestine and the subsequent release of glucose into the bloodstream, taking place at a given initial rate and falling off exponentially with time. An analysis of the model is carried out by the singular perturbation technique in order to derive boundary conditions on the system parameters which identify, in particular, the existence of limit cycles in our model system consistent with the oscillatory patterns often observed in clinical data. We then utilize a sinusoidal term to incorporate the temporal absorption of glucose in order to study the responses in the patients under ambulatory-fed conditions. A numerical investigation is carried out in this case to construct a bifurcation diagram to identify the ranges of parametric values for which chaotic behavior can be expected, leading to interesting biological interpretations.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
lenbury_ruktamatakul_amornsamarnkul_2001_A

The original CellML model was created by:
Catherine Lloyd

[e-mail]
The University of Auckland
The Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..

To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

本模型源自下述论文：
《胰岛素动力学建模：单次口服葡萄糖给药或自由进食状态下的机体响应》

Lenbury Y, Ruktamatakul S, Amornsamarnkul S. Biosystems.
2001 Jan;59(1):15-25. 11226623

摘要：

本文提出了葡萄糖-胰岛素反馈系统的非线性数学模型，该模型已扩展纳入β细胞（beta cell）在人体内维持并调节血浆胰岛素水平的功能。最初，本研究采用葡萄糖的胃肠道吸收项来模拟肠道对葡萄糖的吸收以及后续葡萄糖释放入血的过程，该过程以给定的初始速率启动，并随时间呈指数衰减。本研究采用奇异摄动法对模型进行分析，以推导系统参数的边界条件，尤其可用于确定模型系统中极限环的存在性，这与临床数据中常见的振荡模式相符。随后，我们采用正弦项来模拟葡萄糖的时效性吸收，以研究自由进食状态下患者的机体响应。在此场景下，本研究开展了数值分析以构建分岔图，从而确定可产生混沌行为的参数取值范围，进而得到具有生物学意义的解读。

本模型源自CellML（Cell Markup Language）数据库，并已自动转换为SBML（Systems Biology Markup Language）格式。
原始模型为：lenbury_ruktamatakul_amornsamarnkul_2001_A

原始CellML模型由Catherine Lloyd创建：
[e-mail]
奥克兰大学
生物工程研究所

本模型源自BioModels数据库：经注释的已发表模型数据库（http://www.ebi.ac.uk/biomodels/）。其版权归2005-2011年的BioModels.net团队所有。
在法律允许的最大范围内，本编码模型的所有版权及相关邻接权利已在全球范围内捐赠至公共领域。详细信息请参阅CC0公共领域奉献协议。

简言之，您可完全按照自身认为合适的方式使用本编码模型：可原样使用或修改后使用，可单独使用或嵌入更大的应用场景中，可进行商业或非商业分发，可受限或非受限分发。

若需引用BioModels数据库，请使用以下文献：
Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.