- Author:
- Hanne <Hanne@hanne-nielsens-macbook.local>
- Date:
- 2009-11-05 12:33:29+13:00
- Desc:
- Added keyword, removed non pub med link
- Permanent Source URI:
- https://models.cellml.org/workspace/lenbury_ruktamatakul_amornsamarnkul_2001/rawfile/fa1a05be28285f23a434495a0b92af666f26bbe1/lenbury_ruktamatakul_amornsamarnkul_2001_b.cellml
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<!-- FILE : lenbury_model_2001.xml
CREATED : 18th June 2007
LAST MODIFIED : 18th June 2007
AUTHOR : Catherine Lloyd
Bioengineering Institute
The University of Auckland
MODEL STATUS : This model conforms to the CellML 1.1 Specification.
DESCRIPTION : This file contains a CellML description of Lenbury et al.'s 2001 mathematical model of insulin kinetics.
CHANGES:
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<article>
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<title>Modelling insulin kinetics in response to oral glucose administration</title>
<author>
<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
</affiliation>
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<section id="sec_status">
<title>Model Status</title>
<para>
Please note that this particular variant of the model is an extension of the basic core model. To the three variables described in the core model: plasma insulin concentration (x), glucose concentration (y) and the density of the pancreatic beta cells (z), we are adding a forth variable (u) which describes the temporal glucose absorption by the gastrointestinal tract.
</para>
</section>
<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
The secretion of insulin, and its biological effectiveness in reducing blood glucose levels, is mainly dependent on the number and functional efficiency of the pancreatic beta-cells, and also the degree of peripheral insulin resistance. Diabetes can arise from either a deficiency in insulin secretion or from a resistance to insulin. Several mathematical models have been proposed to try and describe the relationships between the plasma concentrations of glucose and insulin. However, these models are often too complex for the available clinical data; which is usually based on glucose alone and is only for a relatively short time period. The current model described here in CellML is based on the published model of Lenbury <emphasis>et al.</emphasis> (2001) and involves just four variables:
</para>
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<para>Plasma insulin concentration;</para>
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<para>Plasma glucose concentration;</para>
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<para>Pancreatic beta-cell density; and</para>
</listitem>
<listitem>
<para>A term to define gastrointestinal glucose absorption.</para>
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<para>
<informalfigure float="0" id="fig_reaction_diagram">
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<title>model diagram</title>
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<caption>Schematic diagram of the pancreatic beta-cells. Glucose production is by beta-cells and uptake is by gastrointestinal cells. Beta-cell formation and loss represent the rates at which beta-cells replicate and die.</caption>
</informalfigure>
</para>
<para>
The complete original paper reference is cited below:
</para>
<para>
Modeling insulin kinetics: responses to a single oral glucose administration or ambulatory-fed conditions. Yongwimon Lenbury, Sitipong Ruktamatakul, and Somkid Amornsamarnkul, 2001, <emphasis>Mathematical Biosciences</emphasis>, 59, 15-25. <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11226623&query_hl=1&itool=pubmed_docsum">PubMed ID: 11226623</ulink>
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<rdf:Bag rdf:about="rdf:#29051065-d25f-4974-9138-2e9018ad6235">
<rdf:li>insulin</rdf:li>
<rdf:li>pancreas</rdf:li>
<rdf:li>beta cell</rdf:li>
<rdf:li>endocrine</rdf:li>
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<dcterms:W3CDTF>2001-00-00 00:00</dcterms:W3CDTF>
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<dc:publisher>The University of Auckland, Bioengineering Institute</dc:publisher>
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<dcterms:modified rdf:resource="rdf:#fad7737a-fc0d-4daa-ab48-f692f62d1701"/>
<rdf:value>I've added a piecewise equation for "z" such that it can never equal zero. This now solves the NaN problem generated by having a zero as a denominator.</rdf:value>
<cmeta:modifier rdf:resource="rdf:#47b290ae-d7eb-4edf-a5bd-ecac68529ae1"/>
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<vCard:FN>Catherine Lloyd</vCard:FN>
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<dc:title>
Lenbury et al.'s 2001 mathematical model of insulin kinetics.
</dc:title>
<cmeta:bio_entity>pacreatic beta cell</cmeta:bio_entity>
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<rdf:value>The model now runs in PCEnv without producing "NaNs" but I'm still not sure it can recreate the published results.
Also, please note that this particular variant of the model is an extension of the basic core model. To the three variables described in the core model: plasma insulin concentration (x), glucose concentration (y) and the density of the pancreatic beta cells (z), we are adding a forth variable (u) which describes the temporal glucose absorption by the gastrointestinal tract.</rdf:value>
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<dc:title>BioSystems</dc:title>
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<dcterms:W3CDTF>2007-09-03T13:59:03+12:00</dcterms:W3CDTF>
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<dcterms:alternative>glucose absorption</dcterms:alternative>
<dc:title>u</dc:title>
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<dcterms:alternative>pancreatic beta cell density</dcterms:alternative>
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<dc:creator rdf:resource="rdf:#e05e352a-27c4-44bb-9207-40a1be923b12"/>
<dc:title>Mathematical modeling of the hypothalamic-pituitary-adrenal system activity</dc:title>
<bqs:volume>59</bqs:volume>
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<dcterms:alternative>insulin</dcterms:alternative>
<dc:title>x</dc:title>
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<rdf:value>This is the CellML description of Lenbury et al.'s 2001 mathematical model of insulin kinetics.</rdf:value>
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<vCard:Given>Catherine</vCard:Given>
<vCard:Family>Lloyd</vCard:Family>
<vCard:Other>May</vCard:Other>
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<vCard:FN>Catherine Lloyd</vCard:FN>
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<vCard:Given>Somkid</vCard:Given>
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<vCard:Given>Catherine</vCard:Given>
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<dcterms:W3CDTF>2007-06-18T00:00:00+00:00</dcterms:W3CDTF>
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