Use of a Physiologic Pharmacokinetic Model of Glucose Homeostasis for Assessment of Performance Requirements for Improved Insulin Therapies
| Autor: | Colton Ck, Hillman Rs, Sorensen Jt, Soeldner Js |
|---|---|
| Rok vydání: | 1982 |
| Předmět: |
Blood Glucose
medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Models Biological Artificial pancreas Diabetes mellitus Internal medicine Diabetes Mellitus Internal Medicine medicine Hyperinsulinemia Homeostasis Humans Insulin Glucose homeostasis Advanced and Specialized Nursing Glucose tolerance test medicine.diagnostic_test business.industry Glucose Measurement Glucose Tolerance Test medicine.disease Kinetics Endocrinology Liver Regional Blood Flow Blood sugar regulation business |
| Zdroj: | Diabetes Care. 5:148-157 |
| ISSN: | 1935-5548 0149-5992 |
| DOI: | 10.2337/diacare.5.3.148 |
| Popis: | Methods are presented for assessing insulin therapies using a physiologic pharmacokinetic model of glucose homeostasis in man. The model is composed of simultaneous differential equations that represent physiologic compartments and spaces in which glucose and insulin are distributed and undergo metabolic reactions. The model is used to simulate clinical experiments in which blood glucose concentration is controlled by artificial device therapies. Predictions of the theoretical model for responses of normal and diabetic individuals to standard intravenous and oral glucose tolerance tests are compared to clinical data. Reasonable agreement is obtained between predictions of the computer simulations and clinical data for normal individuals. The responses of a diabetic person to oral glucose tolerance tests are simulated by removal of the pancreas from the glucose homeostasis model and introduction of insulin into the model by a prescribed therapy. Model simulations reaffirm expectations concerning the poor blood glucose control attainable by intramuscular insulin injection. Simulations of blood glucose regulation by an artificial pancreas using closed-loop feedback control for controlling insulin delivery rate reveal hyperinsulinemia that results in a net shift in the deposition of a glucose load from liver to peripheral tissues. Simulations of this system in which the time delay for glucose measurement is varied from 1.5 to 30 min show that increases in sensor delay result in progressive loss in glucose regulation, exacerbation of hyperinsulinemia, and increased insulin requirements. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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