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

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 drawbac...

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Publicado en:Medical & Biological Engineering & Computing Vol. 54; no. 9; pp. 1383 - 1399
Autores principales: Vahidi, O., Kwok, K., Gopaluni, R., Knop, F., Kwok, K E, Gopaluni, R B, Knop, F K
Formato: Journal Article
Publicado: Springer Nature Sep2016
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Sep2016
      vid: 54
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      pub: Springer Nature
      place: New York, New York
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        10.1007/s11517-015-1406-4
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        atl: A comprehensive compartmental model of blood glucose regulation for healthy and type 2 diabetic subjects.
      aug:
        au:
          Vahidi, O.
          Kwok, K.
          Gopaluni, R.
          Knop, F.
          Kwok, K E
          Gopaluni, R B
          Knop, F K
        affil: School of Chemical Engineering , Iran University of Science and Technology , Narmak, Tehran Iran
      sug:
        subj:
          Blood Glucose Metabolism
          Models, Biological
          Diabetes Mellitus, Type 2 Blood
          Reproducibility of Results
          Incretins Metabolism
          Glucose Tolerance Test
          Models, Theoretical
          Female
          Glucose Metabolism
          Clinical Trials
          Gastrointestinal System Metabolism
          Male
          Scales
          Female
          Male
      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.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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