β-Cell Glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes.
Open accessAbstract
The relentless decline in beta-cell function frequently observed in type 2 diabetic patients, despite optimal drug management, has variously been attributed to glucose toxicity and lipotoxicity. The former theory posits hyperglycemia, an outcome of the disease, as a secondary force that further damages beta-cells. The latter theory suggests that the often-associated defect of hyperlipidemia is a primary cause of beta-cell dysfunction. We review evidence that patients with type 2 diabetes continually undergo oxidative stress, that elevated glucose concentrations increase levels of reactive oxygen species in beta-cells, that islets have intrinsically low antioxidant enzyme defenses, that antioxidant drugs and overexpression of antioxidant enzymes protect beta-cells from glucose toxicity, and that lipotoxicity, to the extent it can be attributable to hyperlipidemia, occurs only in the context of preexisting hyperglycemia, whereas glucose toxicity can occur in the absence of hyperlipidemia.
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Lipid deposition in pancreatic β-cells is believed to be lipotoxic, decreasing their ability to secrete insulin.
“while in pancreatic β-cells it is believed to be lipotoxic, decreasing their ability to secrete insulin”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Robertson et al., 2004
The section on glucose toxicity and lipotoxicity reports that increased lipid synthesis in islets can inhibit glucose-induced insulin secretion. But it concludes that lipotoxicity occurs only in the context of chronic hyperglycemia, a condition the citing sentence omits. (LLM, conf=0.86)
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- Authors
- Robertson, R. P., Harmon, J., Tran, P. O. T., & Poitout, V.
- Affiliations
- University of Washington (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2004-02-01
- Volume
- 53
- Issue
- suppl_1
- Pages
- S119-S124
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2104622496
- Cited by
- 914
- References
- 60
- Citations by year
- 2026: 25 · 2025: 24 · 2024: 36 · 2023: 38 · 2022: 30 · 2021: 47 · 2020: 50 · 2019: 41 · 2018: 38 · 2017: 45 · 2016: 50 · 2015: 55 · 2014: 56 · 2013: 49 · 2012: 49
- FWCI
- 7.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R-01-DK-38325, R01 DK 58096, R01DK038325, R01DK058096)
- 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 › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Keywords
- beta-cell dysfunction, glucotoxicity, lipotoxicity, oxidative stress, type 2 diabetes, hyperglycemia, hyperlipidemia, reactive oxygen species, antioxidant enzymes, antioxidant drugs, islets
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Humans, Hyperglycemia, Islets of Langerhans, Lipid Peroxides, Oxidative Stress, Rats
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