Type II diabetes, glucose "non-sense," and islet desensitization.
about
Metabolomics applied to the pancreatic isletHexosamine pathway but not interstitial changes mediates glucotoxicity in pancreatic β-cells as assessed by cytosolic Ca2+ response to glucose.Transgenic overexpression of active calcineurin in beta-cells results in decreased beta-cell mass and hyperglycemia.Chronic exposure of HIT cells to high glucose concentrations paradoxically decreases insulin gene transcription and alters binding of insulin gene regulatory protein.A role for glutathione peroxidase in protecting pancreatic beta cells against oxidative stress in a model of glucose toxicity.Reduced capacity and affinity of skeletal muscle for insulin-mediated glucose uptake in noninsulin-dependent diabetic subjects. Effects of insulin therapyEffects of hemipancreatectomy on pancreatic alpha and beta cell function in healthy human donors.Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets.Preservation of insulin mRNA levels and insulin secretion in HIT cells by avoidance of chronic exposure to high glucose concentrations.Prevention of glucose toxicity in HIT-T15 cells and Zucker diabetic fatty rats by antioxidants.The Fas pathway is involved in pancreatic beta cell secretory function.Association of TCF7L2 Genetic Polymorphisms with Type 2 Diabetes Mellitus in the Uygur Population of China.Hyperglycemia-induced B cell toxicity. The fate of pancreatic islets transplanted into diabetic mice is dependent on their genetic background.Geniposide promotes beta-cell regeneration and survival through regulating β-catenin/TCF7L2 pathwayChronic exposure of betaTC-6 cells to supraphysiologic concentrations of glucose decreases binding of the RIPE3b1 insulin gene transcription activator.Differentiation of glucose toxicity from beta cell exhaustion during the evolution of defective insulin gene expression in the pancreatic islet cell line, HIT-T15Prolonged exposure of human beta cells to elevated glucose levels results in sustained cellular activation leading to a loss of glucose regulation.Glycation-dependent, reactive oxygen species-mediated suppression of the insulin gene promoter activity in HIT cells.
P2860
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P2860
Type II diabetes, glucose "non-sense," and islet desensitization.
description
1989 nî lūn-bûn
@nan
1989年の論文
@ja
1989年論文
@yue
1989年論文
@zh-hant
1989年論文
@zh-hk
1989年論文
@zh-mo
1989年論文
@zh-tw
1989年论文
@wuu
1989年论文
@zh
1989年论文
@zh-cn
name
Type II diabetes, glucose "non-sense," and islet desensitization.
@en
type
label
Type II diabetes, glucose "non-sense," and islet desensitization.
@en
prefLabel
Type II diabetes, glucose "non-sense," and islet desensitization.
@en
P356
P1433
P1476
Type II diabetes, glucose "non-sense," and islet desensitization.
@en
P2093
Robertson RP
P304
P356
10.2337/DIAB.38.12.1501
P407
P577
1989-12-01T00:00:00Z