ArticleAmerican journal of physiology. Endocrinology and metabolism2020
Type 2 diabetes: one disease, many pathways.
Article in American journal of physiology. Endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- Serum alkaline phosphatase levels and the risk of new-onset diabetes in hypertensive adults.Cardiovascular diabetology · 2020Trial
- Validation in adult Black and White women of the ISS model for estimating insulin sensitivity and beta-cell function from mixed-meal tests.American journal of physiology. Endocrinology and metabolism · 2026Article
- Quantification of beta-cell carrying capacity in prediabetes.PLoS computational biology · 2026Article
- Is high insulin protective or detrimental? Mathematical modeling reveals the base of the iceberg.American journal of physiology. Endocrinology and metabolism · 2026Article
- Aberrant hepatic glycogenolysis and elevated insulin clearance can lead to major glucose irregularities in type 2 diabetes: insights from system identification.Frontiers in physiology · 2026Article
- Evaluating the role of alpha cell dysregulation in the progression to type 2 diabetes using mathematical simulations.Diabetologia · 2025Article
- α-Glucosidase Inhibition-Guided Network Pharmacology and Molecular Docking Reveal the Antidiabetic Potential ofInternational journal of molecular sciences · 2025Article
- Fatty acids and physical activity are critical for β-cell mass and insulin sensitivity: Pathways to T2D and prevention.Journal of theoretical biology · 2025Article
- Article
- A mathematical model for ketosis-prone diabetes suggests the existence of multiple pancreatic β-cell inactivation mechanisms.bioRxiv : the preprint server for biology · 2025Article
- A Mathematical Model-Derived Disposition Index Without Insulin Validated in Youth With Obesity.The Journal of clinical endocrinology and metabolism · 2025Observational
- Association between alcohol consumption and risk of type 2 diabetes in Japan: a population-base longitudinal cohort study.Scientific reports · 2025Article
- Declining insulin sensitivity is a key pathological contributor to dysglycemia: a longitudinal validation study in the Korean genome and epidemiology study.Frontiers in endocrinology · 2025Article
- Estimating insulin sensitivity and β-cell function from the oral glucose tolerance test: validation of a new insulin sensitivity and secretion (ISS) model.American journal of physiology. Endocrinology and metabolism · 2024Article
- The Role of G Protein-Coupled Receptors and Receptor Kinases in PancreaticPharmacological reviews · 2024Review
- An extended minimal model of OGTT: estimation of α- and β-cell dysfunction, insulin resistance, and the incretin effect.American journal of physiology. Endocrinology and metabolism · 2024Article
- Article
- A multi-scale digital twin for adiposity-driven insulin resistance in humans: diet and drug effects.Diabetology & metabolic syndrome · 2023Article
- Disentangling Dual Threats: Premature Coronary Artery Disease and Early-Onset Type 2 Diabetes Mellitus in South Asians.Journal of the Endocrine Society · 2023Review
- Steady solution and its stability of a mathematical model of diabetic atherosclerosis.Journal of biological dynamics · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is a chronic, progressive disease that calls for longitudinal data and analysis. We introduce a longitudinal mathematical model that is capable of representing the metabolic state of an individual at any point in time during their progression from normal glucose tolerance to type 2 diabetes (T2D) over a period of years. As an application of the model, we account for the diversity of pathways typically followed, focusing on two extreme alternatives, one that goes through impaired fasting glucose (IFG) first and one that goes through impaired glucose tolerance (IGT) first. These two pathways are widely recognized to stem from distinct metabolic abnormalities in hepatic glucose production and peripheral glucose uptake, respectively. We confirm this but go beyond to show that IFG and IGT lie on a continuum ranging from high hepatic insulin resistance and low peripheral insulin resistance to low hepatic resistance and high peripheral resistance. We show that IFG generally incurs IGT and IGT generally incurs IFG on the way to T2D, highlighting the difference between innate and acquired defects and the need to assess patients early to determine their underlying primary impairment and appropriately target therapy. We also consider other mechanisms, showing that IFG can result from impaired insulin secretion, that non-insulin-dependent glucose uptake can also mediate or interact with these pathways, and that impaired incretin signaling can accelerate T2D progression. We consider whether hyperinsulinemia can cause insulin resistance in addition to being a response to it and suggest that this is a minor effect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.