Pancreatic β-Cell Proliferation in Obesity
Open accessAbstract
Because obesity rates have increased dramatically over the past 3 decades, type 2 diabetes has become increasingly prevalent as well. Type 2 diabetes is associated with decreased pancreatic β-cell mass and function, resulting in inadequate insulin production. Conversely, in nondiabetic obesity, an expansion in β-cell mass occurs to provide sufficient insulin and to prevent hyperglycemia. This expansion is at least in part due to β-cell proliferation. This review focuses on the mechanisms regulating obesity-induced β-cell proliferation in humans and mice. Many factors have potential roles in the regulation of obesity-driven β-cell proliferation, including nutrients, insulin, incretins, hepatocyte growth factor, and recently identified liver-derived secreted factors. Much is still unknown about the regulation of β-cell replication, especially in humans. The extracellular signals that activate proliferative pathways in obesity, the relative importance of each of these pathways, and the extent of cross-talk between these pathways are important areas of future study.
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Following the induction of insulin resistance, islet beta-cells can maintain normoglycaemia and metabolic homeostasis by increasing their secretion of insulin and/or by increasing their number.
“Following the induction of insulin resistance, islet beta-cells can maintain normoglycaemia and metabolic homeostasis by increasing their secretion of insulin and/or by increasing their number.49,96,97”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [96]
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Research works printed but not linked: 1
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Why does obesity cause diabetes?
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Endocrine-Exocrine Signaling Drives Obesity-Associated Pancreatic Ductal Adenocarcinoma
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- Authors
- Linnemann, A. K., Baan, M., & Davis, D. B.
- Affiliations
- University of Wisconsin–Madison (US)
- William S. Middleton Memorial Veterans Hospital (US)
- Corresponding author
- Davis, Dawn Belt
- Venue
- Advances in Nutrition
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 5
- Issue
- 3
- Pages
- 278-288
- ISSN
- 2156-5376 (ISSN-L)
- 2161-8313
- PMC
- PMC4013180
- OpenAlex
- W2161222424
- Cited by
- 132
- References
- 96
- Citations by year
- 2026: 9 · 2025: 7 · 2024: 15 · 2023: 11 · 2022: 15 · 2021: 23 · 2020: 9 · 2019: 10 · 2018: 8 · 2017: 7 · 2016: 10 · 2015: 5 · 2014: 3
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Advances in Nutrition (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01BX001880)
- National Institutes of Health (T32OD010423)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK083442, K08DK083442)
- National Center for Research Resources (RR023916, T32RR023916)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- pancreatic beta-cell proliferation, obesity, type 2 diabetes, beta-cell mass, insulin, incretins, hepatocyte growth factor, nutrient signaling, beta-cell proliferation, hyperglycemia
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Humans, Hyperglycemia, Insulin Resistance, Liver, Obesity, Hepatocytes, Receptors, G-Protein-Coupled, Cell Proliferation, Insulin-Secreting Cells, Diet, High-Fat
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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