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MODEL1112110001 - Alvehag2006_OGTT_GlucoseModel_B

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 10.1109/CDC.2006.377...
Alvehag, K.; Martin, C.
The Feedback Control of Glucose: On the road to type II diabetes
Engineering in Medicine and Biology Society, 2008. EMBS 2008. 30th Annual International Conference of the IEEE, On page(s): 5445-5448
  [more]
Model
Original Model: MODEL1112110001.origin
Submitter: Ishan Ajmera
Submission Date: 11 Dec 2011 21:02:44 UTC
Last Modification Date: 11 Dec 2011 21:30:46 UTC
Creation Date: 11 Dec 2011 21:30:46 UTC
Encoders:
bqbiol:isVersionOf Gene Ontology glucose homeostasis
Human Disease Ontology diabetes mellitus
bqbiol:hasTaxon Taxonomy Homo sapiens
Notes

This a model from the article:
The Feedback Control of Glucose: On the road to type II diabetes
Alvehag, K.; Martin, C. Proceedings of 45th IEEE Conference on Decision and Control 2006,685-690
Abstract:
This paper develops a mathematical model for the feedback control of glucose regulation in the healthy human being and is based on the work of Sorensen (1985). The proposed model serves as a starting point for modeling type II diabetes. Four agents - glucose and the three hormones insulin, glucagon, and incretins - are assumed to have an effect on glucose metabolism. By letting compartments represent anatomical organs, the model has a close resemblance to a real human body. Mass balance equations that account for blood flows, exchange between compartments, and metabolic sinks and sources are written, and these result in simultaneous dif- ferential equations that are solved numerically. The metabolic sinks and sources - removing or adding glucose, insulin, glucagon, and incretins - describe physiological processes in the body. These processes function as feedback control systems and have nonlinear behaviors. The results of simulations performed for three different clinical test types indicate that the model is successful in simulating intravenous glucose, oral glucose, and meals containing mainly carbohydrates.

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