β-Cell failure in type 2 diabetes
Open accessAbstract
Type 2 diabetic patients are insulin resistant as a result of obesity and a sedentary lifestyle. Nevertheless, it has been known for the past five decades that insulin response to nutrients is markedly diminished in type 2 diabetes. There is now a consensus that impaired glucose regulation cannot develop without insulin deficiency. First-phase insulin response to glucose is lost very early in the development of type 2 diabetes. Several prospective studies have shown that impaired insulin response to glucose is a predictor of future impaired glucose tolerance (IGT) and type 2 diabetes. Recently discovered type 2 diabetes-risk gene variants influence β-cell function, and might represent the molecular basis for the low insulin secretion that predicts future type 2 diabetes. We believe type 2 diabetes develops on the basis of normal but 'weak'β-cells unable to cope with excessive functional demands imposed by overnutrition and insulin resistance. Several laboratories have shown a reduction in β-cell mass in type 2 diabetes and IGT, whereas others have found modest reductions and most importantly, a large overlap between β-cell masses of diabetic and normoglycemic subjects. Therefore, at least initially, the β-cell dysfunction of type 2 diabetes seems more functional than structural. However, type 2 diabetes is a progressive disorder, and animal models of diabetes show β-cell apoptosis with prolonged hyperglycemia/hyperlipemia (glucolipotoxicity). β-Cells exposed in vitro to glucolipotoxic conditions show endoplasmic reticulum (ER) and oxidative stress. ER stress mechanisms might participate in the adaptation of β-cells to hyperglycemia, unless excessive. β-Cells are not deficient in anti-oxidant defense, thioredoxin playing a major role. Its inhibitor, thioredoxin-interacting protein (TXNIP), might be important in leading to β-cell apoptosis and type 2 diabetes. These topics are intensively investigated and might lead to novel therapeutic approaches. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00094.x, 2011).
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Regardless of the treatment regime, longitudinal studies in humans have demonstrated that beta-cell function generally deteriorates over time.
“Regardless of the treatment regime, longitudinal studies in humans have demonstrated that beta-cell function generally deteriorates over time.49,50”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [50]
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- Leibowitz, G., Kaiser, N., & Cerasi, E.
- Affiliations
- Hebrew University of Jerusalem (IL)
- Corresponding author
- Cerasi, Erol
- Venue
- Journal of Diabetes Investigation
- Publisher
- Wiley
- Published
- 2011-01-21
- Volume
- 2
- Issue
- 2
- Pages
- 82-91
- ISSN
- 2040-1116 (ISSN-L)
- PMC
- PMC4015541
- OpenAlex
- W1710400459
- Cited by
- 78
- References
- 91
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 8 · 2023: 2 · 2022: 1 · 2021: 7 · 2020: 10 · 2019: 6 · 2018: 3 · 2017: 11 · 2016: 10 · 2015: 6 · 2014: 2 · 2013: 4 · 2012: 3
- FWCI
- 0.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Diabetes Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- beta-cell dysfunction, type 2 diabetes, insulin resistance, impaired glucose tolerance, first-phase insulin response, beta-cell mass, glucolipotoxicity, beta-cell apoptosis, endoplasmic reticulum stress, oxidative stress, thioredoxin, TXNIP, genetic risk variants
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