A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects

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Standard

A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. / Vahidi, O; Kwok, K E; Gopaluni, R B; Knop, F K.

In: Medical & Biological Engineering & Computing, Vol. 54, No. 9, 2016, p. 1383-1398.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vahidi, O, Kwok, KE, Gopaluni, RB & Knop, FK 2016, 'A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects', Medical & Biological Engineering & Computing, vol. 54, no. 9, pp. 1383-1398. https://doi.org/10.1007/s11517-015-1406-4

APA

Vahidi, O., Kwok, K. E., Gopaluni, R. B., & Knop, F. K. (2016). A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. Medical & Biological Engineering & Computing, 54(9), 1383-1398. https://doi.org/10.1007/s11517-015-1406-4

Vancouver

Vahidi O, Kwok KE, Gopaluni RB, Knop FK. A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. Medical & Biological Engineering & Computing. 2016;54(9):1383-1398. https://doi.org/10.1007/s11517-015-1406-4

Author

Vahidi, O ; Kwok, K E ; Gopaluni, R B ; Knop, F K. / A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. In: Medical & Biological Engineering & Computing. 2016 ; Vol. 54, No. 9. pp. 1383-1398.

Bibtex

@article{c199677978e44dafb8fb2f76cd39ac76,
title = "A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects",
abstract = "We have expanded a former compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. The former model was a detailed physiological model which considered the interactions of three substances, glucose, insulin and glucagon on regulating the blood sugar. The main drawback of the former model was its restriction on the route of glucose entrance to the body which was limited to the intravenous glucose injection. To handle the oral glucose intake, we have added a model of glucose absorption in the gastrointestinal tract to the former model to address the resultant variations of blood glucose concentrations following an oral glucose intake. Another model representing the incretins production in the gastrointestinal tract along with their hormonal effects on boosting pancreatic insulin production is also added to the former model. We have used two sets of clinical data obtained during oral glucose tolerance test and isoglycemic intravenous glucose infusion test from both type 2 diabetic and healthy subjects to estimate the model parameters and to validate the model results. The estimation of model parameters is accomplished through solving a nonlinear optimization problem. The results show acceptable precision of the estimated model parameters and demonstrate the capability of the model in accurate prediction of the body response during the clinical studies.",
author = "O Vahidi and Kwok, {K E} and Gopaluni, {R B} and Knop, {F K}",
year = "2016",
doi = "10.1007/s11517-015-1406-4",
language = "English",
volume = "54",
pages = "1383--1398",
journal = "Medical and Biological Engineering and Computing",
issn = "0140-0118",
publisher = "Springer",
number = "9",

}

RIS

TY - JOUR

T1 - A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects

AU - Vahidi, O

AU - Kwok, K E

AU - Gopaluni, R B

AU - Knop, F K

PY - 2016

Y1 - 2016

N2 - We have expanded a former compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. The former model was a detailed physiological model which considered the interactions of three substances, glucose, insulin and glucagon on regulating the blood sugar. The main drawback of the former model was its restriction on the route of glucose entrance to the body which was limited to the intravenous glucose injection. To handle the oral glucose intake, we have added a model of glucose absorption in the gastrointestinal tract to the former model to address the resultant variations of blood glucose concentrations following an oral glucose intake. Another model representing the incretins production in the gastrointestinal tract along with their hormonal effects on boosting pancreatic insulin production is also added to the former model. We have used two sets of clinical data obtained during oral glucose tolerance test and isoglycemic intravenous glucose infusion test from both type 2 diabetic and healthy subjects to estimate the model parameters and to validate the model results. The estimation of model parameters is accomplished through solving a nonlinear optimization problem. The results show acceptable precision of the estimated model parameters and demonstrate the capability of the model in accurate prediction of the body response during the clinical studies.

AB - We have expanded a former compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects. The former model was a detailed physiological model which considered the interactions of three substances, glucose, insulin and glucagon on regulating the blood sugar. The main drawback of the former model was its restriction on the route of glucose entrance to the body which was limited to the intravenous glucose injection. To handle the oral glucose intake, we have added a model of glucose absorption in the gastrointestinal tract to the former model to address the resultant variations of blood glucose concentrations following an oral glucose intake. Another model representing the incretins production in the gastrointestinal tract along with their hormonal effects on boosting pancreatic insulin production is also added to the former model. We have used two sets of clinical data obtained during oral glucose tolerance test and isoglycemic intravenous glucose infusion test from both type 2 diabetic and healthy subjects to estimate the model parameters and to validate the model results. The estimation of model parameters is accomplished through solving a nonlinear optimization problem. The results show acceptable precision of the estimated model parameters and demonstrate the capability of the model in accurate prediction of the body response during the clinical studies.

U2 - 10.1007/s11517-015-1406-4

DO - 10.1007/s11517-015-1406-4

M3 - Journal article

C2 - 26493377

VL - 54

SP - 1383

EP - 1398

JO - Medical and Biological Engineering and Computing

JF - Medical and Biological Engineering and Computing

SN - 0140-0118

IS - 9

ER -

ID: 150706269