- Author:
- Hanne <Hanne@hanne-nielsens-macbook.local>
- Date:
- 2009-12-09 12:19:39+13:00
- Desc:
- Added images in ai and svg format
- Permanent Source URI:
- https://staging.physiomeproject.org/workspace/li_kuang_mason_2006/rawfile/bf610d37d225430b6368835a9f98845081d59e22/li_kuang_mason_2006.cellml
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<title>Modelling the glucose-insulin regulatory system and ultradian insulin secretory oscillations</title>
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<title>Model Structure</title>
<para>
The human body needs to maintain a relatively steady blood glucose concentration, within the narrow range of 70-109mg/dl, and it has to accommodate large fluctuations in the rates of glucose production and utilisation. The two main sources of glucose production are the digestion of dietary carbohydrates, and also the break down of the storage carbohydrate glycogen in the liver. Glucose utilisation can be insulin-independent - for example in the brain and by nerve cells, or insulin-dependent - for example in muscle, fat and in other tissues. Insulin plays a pivotal role in the maintenance of blood glucose homeostasis. Elevated glucose concentrations stimulate the pancreatic beta cells to secrete insulin. In turn, this inhibits the release of glucose from the liver, and enhances glucose consumption in muscle, fat and other tissues, effectively reducing the blood glucose level. As glucose levels fall, pancreatic insulin secretion ceases. The secretion of insulin in the glucose-insulin endocrine metabolic system occurs in an oscillatory manner over a time range of 50-150 minutes, and are usually referred to as ultradian oscillations. The liver and kidney represent the principal sites of insulin degradation and clearance, and any residual insulin can also be cleared by other tissues.
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<para>
If the ability of the pancreatic beta cells to produce insulin is impaired, or if the insulin produced is unable to induce glucose uptake and utilisation, diabetes mellitus is likely to develop. Diabetes is associated with several complications, including an increased risk of cardiovascular disease and retinal damage. Further, concurrent with the obesity <emphasis>epidemic</emphasis> of the developed world, the incidence of diabetes is increasing dramatically. In combination, these factors provide a huge incentive to researchers to better understand the factors underlying the development of diabetes, with the ultimate aim of improved diagnosis and effective treatment.
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To this end, mathematical models of the glucose-insulin regulatory system represent a potentially useful tool in improving our understanding of the pathogenesis of diabetes. The model presented here (and summarised in the figure below) was developed by Li <emphasis>et al.</emphasis> (2006). It builds on previously published models by adding two time delays to the system of equations; one representing the time it takes for newly synthesised insulin to cross the endothelial barrier into the circulation, and the other represents the delayed effect of insulin on hepatic glucose production.
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<caption>Schematic diagram of the glucose-insulin regulatory system model. The dotted lines indicate that elevated glucose concentration stimulates insulin synthesis and secretion by the pancreatic beta-cells, and also insulin promotes glucose utilisation in muscle, fat and other tissues.</caption>
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The original paper reference is cited below:
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<para>
Modeling the glucose-insulin regulatory system and ultradian insulin secretory oscillations with two explicit time delays, Jiaxu Li, Yang Kuang, and Clinton C. Mason, 2006, Journal of Theoretical Biology, 242, 722-735. <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16712872&query_hl=1&itool=pubmed_docsum">PubMed ID: 16712872</ulink>
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Unfortunately, the two time delays included in the original published model have not been included in the current CellML description of the model. At present, there is no way to express time delays in CellML.
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<vCard:FN>Catherine Lloyd</vCard:FN>
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<dc:title>Journal of Theoretical Biology</dc:title>
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<vCard:Given>Jiaxu</vCard:Given>
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This is the CellML description of Li et al.'s 2006 mathematical model of the glucose-insulin regulatory system and ultradian insulin secretory oscillations. Note that the two time delays - tau1 and tau2 - included in the original published model have not been included in the current CellML description of the model. At present, there is no way for the CellML to handle these delays.
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<vCard:Given>Catherine</vCard:Given>
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