ArticleEndocrinology2016
A Mathematical Model of the Pathogenesis, Prevention, and Reversal of Type 2 Diabetes.
Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 93 citations in OpenAlex.
- 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
- Systematic Review: Exploring Inter-Species Variability in Diabetes Mellitus for Translational Medicine.Life (Basel, Switzerland) · 2025Review
- 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
- The Causal Role of Ectopic Fat Deposition in the Pathogenesis of Metabolic Syndrome.International journal of molecular sciences · 2024Review
- 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
- Steady solution and its stability of a mathematical model of diabetic atherosclerosis.Journal of biological dynamics · 2023Article
- A data-driven computational model for obesity-driven diabetes onset and remission through weight loss.iScience · 2023Article
- A simple modeling framework for prediction in the human glucose-insulin system.Chaos (Woodbury, N.Y.) · 2023Article
- Glucokinase Inhibition: A Novel Treatment for Diabetes?Diabetes · 2023Review
- Modeling the progression of Type 2 diabetes with underlying obesity.PLoS computational biology · 2023Article
- Induction of remission in diabetes by lowering blood glucose.Frontiers in endocrinology · 2023Article
- Article
- Integrated experimental-computational analysis of a HepaRG liver-islet microphysiological system for human-centric diabetes research.PLoS computational biology · 2022Article
- Dynamics of thyroid diseases and thyroid-axis gland masses.Molecular systems biology · 2022Article
- Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes.Diabetes · 2022Article
- The Relationship Between Lipoproteins and Insulin Sensitivity in Youth With Obesity and Abnormal Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2022Observational
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Type 2 diabetes (T2D) is generally thought to result from the combination of 2 metabolic defects, insulin resistance, which increases the level of insulin required to maintain glucose within the normal range, and failure of insulin-secreting pancreatic β-cells to compensate for the increased demand. We build on a mathematical model pioneered by Topp and colleagues to elucidate how compensation succeeds or fails. Their model added a layer of slow negative feedback to the classic insulin-glucose loop in the form of a slow, glucose-dependent birth and death law governing β-cell mass. We add to that model regulation of 2 aspects of β-cell function on intermediate time scales. The model quantifies the relative contributions of insulin action and insulin secretion defects to T2D and explains why prevention is easier than cure. The latter is a consequence of a threshold separating the normoglycemic and diabetic states (bistability), which also underlies the success of bariatric surgery and acute caloric restriction in rapidly reversing T2D. The threshold concept gives new insight into "Starling's Law of the Pancreas," whereby insulin secretion is higher for prediabetics and early diabetics than for normal individuals.
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What OpenQuestion holds
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.