title: Acute hyperglycemia rapidly suppresses endothelium-dependent arterial dilation in first-degree relatives of type 2 diabetic patients.
abstract: OBJECTIVE
  Previous studies showed that endothelium-dependent arterial dilation is impaired in first-degree relatives of type 2 diabetes in the fasting state. In the present study, we examined whether endothelial dysfunction occurs when acute hyperglycemia is induced by oral glucose loading in this cohort.
  
  
  METHODS
  This study included 32 normal glucose tolerant subjects. Of them, 17 with a family history (FH) of type 2 diabetic parents (FH+) and 15 with no first-degree relative with diabetes or coronary artery disease (FH-). The examination of vascular function was performed in fasting state and repeated 1 and 2 hours after a 75-g oral glucose loading by high resolution ultrasound.
  
  
  RESULTS
  Endothelium- dependent arterial dilation in FH+ group were significantly lower than those in FH- before and after oral glucose loading (5.12+/-0.61% vs 6.03+/-0.56%, fasting; 4.0+/-0.65% vs 5.70+/-0.42%, 1 h; 4.43+/-0.61% vs 5.82+/-0.67% 2 h, p<0.05 each). In FH+ group, endothelium-dependent arterial dilation decreased significantly at 60 min (4.0+/-0.65% vs 5.12+/-0.61%, p<0.01) and increased markedly from 60 min at 120 min (4.43+/-0.61% vs 4.0+/-0.65%, p<0.05), which was still significantly lower than baseline (4.43+/-0.61% vs 5.12+/-0.61%, p<0.01) . In FH- group, however, the arterial dilation did not differ significantly among the three time points (p 0.05). In multiple regression analysis, endothelium-dependent arterial dilation was significantly correlated to FH+(r=-0.302, p<0.01). In addition, endothelium-dependent arterial dilation showed a correlation with plasma glucose (r=-0.460, p<0.01) and TBARS (r=-0.382, p<0.01) during OGTT in FH+ subjects.
  
  
  CONCLUSIONS
  Significant endothelial dysfunction is present in the fasting state, hyperglycemia in response to oral glucose loading rapidly suppresses endothelium-dependent arterial dilation in FH+ subjects, probably through increased production of oxygen-derived free radicals.
authors.affiliation: Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei Province, PR China. Guangda64@hotmail.com
authors.forename: G D
authors.initials: GD
authors.lastname: Xiang
authors.forename: H L
authors.initials: HL
authors.lastname: Sun
authors.forename: J
authors.initials: J
authors.lastname: Hou
authors.forename: L
authors.initials: L
authors.lastname: Yue
authors.forename: L
authors.initials: L
authors.lastname: Xu
mesh_terms: D000208:Acute Disease; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism; D004730:Endothelium, Vascular / Q000502:physiology*; D005192:Family Health; D005260:Female; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014463:Ultrasonography; D014664:Vasodilation / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D017392:Thiobarbituric Acid Reactive Substances; C517652:hemoglobin A1c protein, human