肠促胰岛素
内科学
内分泌学
2型糖尿病
胰高血糖素
胰岛素
胰岛素抵抗
胰高血糖素样肽-1
医学
糖尿病
激素
作者
Vijaya Subramanian,Jonatan I. Bagger,Vinayak Harihar,Jens J. Holst,Filip K. Knop,Tina Villsbøll
出处
期刊:American Journal of Physiology-endocrinology and Metabolism
[American Physiological Society]
日期:2024-02-01
卷期号:326 (2): E182-E205
被引量:1
标识
DOI:10.1152/ajpendo.00278.2023
摘要
Loss of insulin sensitivity, α- and β-cell dysfunction, and impairment in incretin effect have all been implicated in the pathophysiology of type 2 diabetes (T2D). Parsimonious mathematical models are useful in quantifying parameters related to the pathophysiology of T2D. Here, we extend the minimum model developed to describe the glucose-insulin-glucagon dynamics in the isoglycemic intravenous glucose infusion (IIGI) experiment to the oral glucose tolerance test (OGTT). The extended model describes glucose and hormone dynamics in OGTT including the contribution of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide-1 (GLP-1), to insulin secretion. A new function describing glucose arrival from the gut is introduced. The model is fitted to OGTT data from eight individuals with T2D and eight weight-matched controls (CS) without diabetes to obtain parameters related to insulin sensitivity, β- and α-cell function. The parameters, i.e., measures of insulin sensitivity,
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