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Cited by 330Pancreatic function and diabetesDiabetes Management and ResearchDiabetes and associated disorders

The DOI matches its Crossref record; 58 of the 60 references it cites were found in a registry or an index.

A model of β-cell mass, insulin, and glucose kinetics: pathways to diabetes

TOPP, BRIAN, PROMISLOW, KEITH, DEVRIES, GERDA, MIURA, ROBERT M, FINEGOOD, DIANE T·2000·Journal of Theoretical Biology
DOI 10.1006/jtbi.2000.2150
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Abstract

Diabetes is a disease of the glucose regulatory system that is associated with increased morbidity and early mortality. The primary variables of this system are beta-cell mass, plasma insulin concentrations, and plasma glucose concentrations. Existing mathematical models of glucose regulation incorporate only glucose and/or insulin dynamics. Here we develop a novel model of beta -cell mass, insulin, and glucose dynamics, which consists of a system of three nonlinear ordinary differential equations, where glucose and insulin dynamics are fast relative to beta-cell mass dynamics. For normal parameter values, the model has two stable fixed points (representing physiological and pathological steady states), separated on a slow manifold by a saddle point. Mild hyperglycemia leads to the growth of the beta -cell mass (negative feedback) while extreme hyperglycemia leads to the reduction of the beta-cell mass (positive feedback). The model predicts that there are three pathways in prolonged hyperglycemia: (1) the physiological fixed point can be shifted to a hyperglycemic level (regulated hyperglycemia), (2) the physiological and saddle points can be eliminated (bifurcation), and (3) progressive defects in glucose and/or insulin dynamics can drive glucose levels up at a rate faster than the adaptation of the beta -cell mass which can drive glucose levels down (dynamical hyperglycemia).

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Crossref · 10.1006/jtbi.2000.2150

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Metadata

Authors
TOPP, B., PROMISLOW, K., DEVRIES, G., MIURA, R. M., & FINEGOOD, D. T.
Affiliations
  • Simon Fraser University (CA)
  • University of Alberta (CA)
  • University of British Columbia (CA)
ORCID
Venue
Journal of Theoretical Biology
Publisher
Elsevier BV
Published
2000-10
Volume
206
Issue
4
Pages
605-619
ISSN
0022-5193 (ISSN-L)
DOI
10.1006/jtbi.2000.2150
OpenAlex
W2002062638
Cited by
330
References
60
Citations by year
2026: 25 · 2025: 30 · 2024: 23 · 2023: 17 · 2022: 22 · 2021: 20 · 2020: 21 · 2019: 13 · 2018: 11 · 2017: 5 · 2016: 16 · 2015: 19 · 2014: 13 · 2013: 12 · 2012: 9
FWCI
3.60
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Theoretical Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
beta-cell mass, insulin dynamics, glucose kinetics, diabetes mellitus, glucose regulation, hyperglycemia, slow manifold, saddle points, bifurcation, negative feedback, positive feedback, nonlinear ordinary differential equations
MeSH terms
Blood Glucose, Diabetes Mellitus, Humans, Insulin, Islets of Langerhans, Models, Biological, Nonlinear Dynamics, Cell Size

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