![]() A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees of beta-cell deficiency and insulin resistance. The steady-state of basal plasma glucose and insulin concentrations is determined by their interaction in a feedback loop between the liver and the beta-cells, thereby maintaining an effective insulin action in the liver and at the periphery. 6 Therefore, individuals with this type of diabetes usually have relative insulin deficiency due to progressive decline of beta-cell insulin secretion frequently on the background of peripheral insulin resistance. At the time of diagnosis of T2D, decompensation becomes stable, making beta-cells unable to compensate for insulin resistance due to reduced beta-cell mass with subsequent rapid and higher blood glucose concentration. 4Įvidence from the Whitehall II cohort study 5 indicated that insulin resistance and intermittent hyperglycemia were found about 13 years before the diagnosis of T2D, and unstable decompensation of beta-cell function started about 2–6 years before the diagnosis at a time when more sustained hyperglycemia at pre-diabetes range developed in the face of worsening insulin resistance. 3 Deterioration of beta-cell function is reflected by elevated fasting blood glucose and hemoglobin A1c (HbA1c), and reduced insulin secretion. 2 The mediating pathways of hyperglycemia that contribute to beta-cell dysfunction include organs associated with insulin resistance like the liver, skeletal muscle and adipose tissue, leading ultimately to a progressive decline of beta-cell function in the face of insulin resistance. 1 Although patients with T2D often secrete large amounts of insulin, insulin sensitivity and secretion are imbalanced, and the increased concentration of insulin is not sufficient to meet the increased demands imposed by obesity and insulin resistance. It broadly encompasses any form of diabetes that is not type 1 diabetes, Maturity Onset Diabetes of the Young (MODY) or secondary diabetes. Type 2 diabetes (T2D) tends to have a complex etiology that cannot be encapsulated by a single feature. How might these results change the focus of research or clinical practice?įor adult patients with newly diagnosed diabetes, identifying the clinical phenotype from a single fasting blood sample using the Homeostasis Model Assessment-2 computer-based modeling, together with clinical characteristics and biomarker measures, may allow more individualized and precision medicine treatment of diabetes. We also considered early detection of microvascular disease and prediction of diabetes-related cardiovascular complications. Using data-driven cluster analysis, we identified three phenotypes of newly diagnosed diabetes in adults, based on estimation of insulin secretion and insulin sensitivity, key clinical characteristics, and biomarker measures. T2D can develop at two extremes, with patients having either beta-cell failure or insulin resistance. It is characterized by varying degrees of insulin resistance and insulin deficiency. Type 2 diabetes (T2D) is a common chronic disease with complex etiology and high heterogeneity. Significance of this study What is already known about this subject? ![]()
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