title: Involvement of oxidative stress in suppression of insulin biosynthesis under diabetic conditions.
abstract: Type 2 diabetes is characterized by pancreatic β-cell dysfunction and insulin resistance, and the number of patients has markedly increased worldwide. In the diabetic state, hyperglycemia per se and subsequent induction of oxidative stress decrease insulin biosynthesis and secretion, leading to the aggravation of Type 2 diabetes. In addition, there is substantial reduction in expression and/or activities of several insulin gene transcription factors. This process is known as β-cell glucose toxicity, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress explains, at least in part, the molecular mechanism for β-cell glucose toxicity, which is often observed in Type 2 diabetes.
authors.affiliation: Department of Metabolic Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. kaneto@endmet.med.osaka-u.ac.jp.
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kaneto
authors.forename: Taka-Aki
authors.initials: TA
authors.lastname: Matsuoka
mesh_terms: D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology; D005947:Glucose / Q000633:toxicity; D006801:Humans; D007328:Insulin / Q000096:biosynthesis*; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D007328:Insulin; D017382:Reactive Oxygen Species; D014157:Transcription Factors; D048031:JNK Mitogen-Activated Protein Kinases; D005947:Glucose