ArticleDiabetology international2017
Exploring the molecular mechanisms underlying α- and β-cell dysfunction in diabetes.
Article in Diabetology international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- α-cell SLC38A5 supports amino acid-induced α-cell proliferation and glucagon secretion.Frontiers in endocrinology · 2026Article
- An update on current type 2 diabetes mellitus (T2DM) druggable targets and drugs targeting them.Molecular diversity · 2025Review
- Impact of Preoperative Diabetes on Insulin Management and Nutritional Status After Total or Completion Pancreatectomy.Annals of surgical oncology · 2025Article
- Nickel Sulfate-Induced GSIS Injury in MIN6 Cells by Activating the JNK Pathway Through Oxidative Stress.Biological trace element research · 2025Article
- Newly discovered knowledge pertaining to glucagon and its clinical applications.Journal of diabetes investigation · 2023Review
- Effect of guanylin peptides on pancreas steatosis and function in experimental diet-induced obesity and after bariatric surgery.Frontiers in endocrinology · 2023Article
- Evaluation of Trace Elements Levels and Construction of Auxiliary Prediction Model in Patients with Diabetes Ketoacidosis in Type 1 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Management of Diabetic Ketoacidosis in Children and Adolescents with Type 1 Diabetes Mellitus.Paediatric drugs · 2020Review
- Involvement of Estrogen Receptor-α in the Activation of Nrf2-Antioxidative Signaling Pathways by Silibinin in Pancreatic β-Cells.Biomolecules & therapeutics · 2020Article
- Consistency of plasma glucagon levels in patients with type 1 diabetes after a 1-year period.Journal of diabetes investigation · 2020Article
- Alpha the versatile: Guardians of the islets.Journal of diabetes investigation · 2019Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic islet dysfunction, including impaired insulin secretion in β cells and dysregulated glucagon secretion in α cells, is the chief pathology of diabetes. In β cells, oxidative stress, evoked by chronic hyperglycemia, was found to induce dysfunction of a critical transcription factor, PDX1, caused by its nucleocytoplasmic translocation via interactions with the insulin and JNK signaling pathways and another transcription factor, FOXO1. The significance of α-cell insulin signaling in the physiological and pathological regulation of α-cell biology was demonstrated in α-cell-specific insulin receptor knockout mice, which exhibited dysregulated glucagon secretion. Moreover, a high-glucose load directly induced excessive glucagon secretion in a glucagon-secreting cell line and isolated islets, together with impairment of insulin signaling. These findings indicate that disordered insulin signaling is central to the pathophysiology of islet dysfunction in both α and β cells. On the other hand, certain beneficial effects of GLP-1 on dysfunctional α and β cells indicate that it has therapeutic potential for diabetes patients who exhibit insulin resistance in islets. These studies, involving basic medical research approaches, have-at least in part-clarified the molecular mechanisms underlying α- and β-cell dysfunction in diabetes, and offer important clues that should aid the development of future therapeutic approaches to the disease.
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