β-Cell deterioration during diabetes: what’s in the gun?
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Clinical management of patients with type 2 diabetes (T2D) successfully prevents extreme hyperglycemia but does not precisely control glucose levels throughout the day. The pathogenesis of T2D is akin to a double-barrel shotgun. The first trigger causes an explosion that sets genetic expression of the disease in motion; the second trigger discharges a host of environmental factors that worsen its clinical course. Candidate shells include glucolipotoxicity, cytokines, oxidative and endoplasmic reticulum stress and insulin resistance. This review considers how each candidate adversely impacts beta-cell function to create the downward spiral of glycemic control. Their roles in pathogenesis raise possibilities for new drug therapies designed to protect against adverse effects of residual hyperglycemia in patients treated with conventional drugs.
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Chronically increased ROS production can induce β-cell death and result in gradual onset of diabetes.
“Chronically increased ROS production could also induce -cell death and result in gradual onset of diabetes (249 -253).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [253]
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- Authors
- Robertson, R. P.
- Affiliations
- Pacific Northwest Research Institute (US)
- Corresponding author
- Robertson, R. Paul
- ORCID
- Robertson, R. Paul
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 20
- Issue
- 8
- Pages
- 388-393
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC2756315
- OpenAlex
- W1967287226
- Cited by
- 93
- References
- 59
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 6 · 2021: 4 · 2020: 2 · 2019: 9 · 2018: 7 · 2017: 2 · 2016: 6 · 2015: 11 · 2014: 9 · 2013: 9 · 2012: 8
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- U.S. Public Health Service (R01 85325)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK038325, R01DK039994)
- 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, type 2 diabetes pathogenesis, glucolipotoxicity, cytokines, oxidative stress, endoplasmic reticulum stress, insulin resistance, glycemic control, beta-cell protection
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Models, Biological, Cytokines, Oxidative Stress, Insulin-Secreting Cells
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