2014
DOI: 10.4236/jbise.2014.76035
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Mathematical Modelling and Simulation of <i>β</i>-Cell Mass, Insulin and Glucose Dynamics: Effect of Genetic Predisposition to Diabetes

Abstract: Worldwide, diabetes is affecting 370 million people, causing nearly five million deaths and absorbing more than 471 billion USD per year. Mathematical models have been developed to simulate, analyse and understand the dynamics of β-cells, insulin and glucose. In this paper, we consider the effect of genetic predisposition to diabetes on dynamics of β-cells, glucose and insulin. We assume that the β-cell dynamics is governed by the differential equation:

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Cited by 25 publications
(21 citation statements)
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“…These parameters were applied to the mathematical model for the pancreas–muscle–liver MPS, and the glucose and insulin concentration were predicted. When the glucose production rate of the liver (Pr glu ) of 10 mM/hr, and an insulin clearance rate (Cl ins ) of 200 mU/hr were applied to the model, which was determined by fitting to the concentration profiles from the literature, the predicted concentration profile of glucose in the blood compartment matched the glucose concentration profile in the blood the human reported in the literature (Figure c‐i, S1; Bergman et al, ; Boutayeb et al, ). These results suggest that the addition of the liver compartment enabled more physiologically relevant description of glucose dynamics than the model having the pancreas and the muscle only.…”
Section: Resultsmentioning
confidence: 92%
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“…These parameters were applied to the mathematical model for the pancreas–muscle–liver MPS, and the glucose and insulin concentration were predicted. When the glucose production rate of the liver (Pr glu ) of 10 mM/hr, and an insulin clearance rate (Cl ins ) of 200 mU/hr were applied to the model, which was determined by fitting to the concentration profiles from the literature, the predicted concentration profile of glucose in the blood compartment matched the glucose concentration profile in the blood the human reported in the literature (Figure c‐i, S1; Bergman et al, ; Boutayeb et al, ). These results suggest that the addition of the liver compartment enabled more physiologically relevant description of glucose dynamics than the model having the pancreas and the muscle only.…”
Section: Resultsmentioning
confidence: 92%
“…An insulin secretion model of the pancreas was based on the literature (Boutayeb, Lamlili, Boutayeb, & Derouich, ), and the equation for the model was expressed as follows: VbloodinpancreasitalicdIitalicdt=VpancreasRinsGKins+G,where V blood in pancreas is the volume of blood in pancreas, I is the concentration of insulin, t is time, V pancreas is volume of pancreas, G is concentration of glucose, R ins is maximum rate of insulin secretion, and K ins is constant of insulin secretion model.…”
Section: Methodsmentioning
confidence: 99%
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“…Hernandez et al proposed an extension of the Topp model by adding the surface insulin receptor dynamics [10]. Boutayeb et al extended Topps model by stressing the effect of genetic predisposition to diabetes [11].…”
Section: Introductionmentioning
confidence: 99%
“…Our model is based on mathematical models published by Boutayeb et al [11], Roy et al [8] and Hernandez et al [10].…”
Section: Introductionmentioning
confidence: 99%