Uric acid‐induced pancreatic β-cell dysfunction
| Autor: | Asghar Ghasemi |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Endocrinology Diabetes and Metabolism Inflammation Hyperuricemia Review Type 2 diabetes medicine.disease_cause lcsh:Diseases of the endocrine glands. Clinical endocrinology Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Insulin resistance Insulin-Secreting Cells Internal medicine Diabetes mellitus Insulin Secretion medicine Animals Humans Pancreatic β-cell lcsh:RC648-665 Cell Death business.industry General Medicine Uricosuric Agents medicine.disease 030104 developmental biology Endocrinology Diabetes Mellitus Type 2 chemistry 030220 oncology & carcinogenesis Uric acid medicine.symptom business Oxidative stress |
| Zdroj: | BMC Endocrine Disorders, Vol 21, Iss 1, Pp 1-5 (2021) BMC Endocrine Disorders |
| ISSN: | 1472-6823 |
| Popis: | Hyperuricemia is associated with insulin resistance, pancreatic β-cell dysfunction and consequently with development of type 2 diabetes. Although a direct relationship between high levels of uric acid (UA) and the development of diabetes is still a controversial issue, there is some evidence that strongly points to pancreatic β-cells damage as a result of high serum UA levels. Here, the mechanisms underlying UA-induced β-cell damage are discussed. Available literature indicates that UA can decrease glucose-stimulated insulin secretion and cause β-cell death. The mechanisms underlying these effects are UA-induced oxidative stress and inflammation within the β-cells. UA also stimulates inducible nitric oxide (NO) synthase (iNOS) gene expression leading to NO-induced β-cell dysfunction. Thus hyperuricemia may potentially cause β-cell dysfunction, leading to diabetes. It may be hypothesized that in hyperuricemic subjects, UA-lowering drugs may be beneficial in preventing diabetes. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|