Simultaneous control of hyperglycemia and oxidative stress normalizes endothelial function in type 1 diabetes.
OBJECTIVE
Previous studies have shown that in type 1 diabetes endothelial dysfunction persists even when glycemia is normalized. Moreover, oxidative stress has recently been demonstrated to be the mediator of hyperglycemia-induced endothelial dysfunction.


METHODS
Thirty-six type 1 diabetic patients and 12 control subjects were enrolled. The diabetic patients were divided into three groups. The first group was treated for 24 h with insulin, achieving a near-normalization of glycemia. After 12 h of this treatment, vitamin C was added for the remaining 12 h. The second group was treated for 24 h with vitamin C. After 12 h of this treatment, insulin was started, with achievement of near-normalization of glycemia for the remaining 12 h. The third group was treated for 24 h with both vitamin C and insulin, achieving near-normalization of glycemia.


RESULTS
Neither normalization of glycemia nor vitamin C treatment alone was able to normalize endothelial dysfunction or oxidative stress. However, a combination of insulin and vitamin C normalized endothelial dysfunction and decreased oxidative stress to normal levels.


CONCLUSIONS
This study suggests that long-lasting hyperglycemia in type 1 diabetic patients induces permanent alterations in endothelial cells, which may contribute to endothelial dysfunction by increased oxidative stress even when hyperglycemia is normalized.
Ceriello
Antonio
A
Centre of Excellence in Diabetes and Endocrinology, University Hospital of Coventry and Warwickshire, Warwick Medical School, University of Warwick, Coventry, UK. antonio.ceriello@warwick.ac.uk
Kumar
Sudhesh
S
Piconi
Ludovica
L
Esposito
Katerine
K
Giugliano
Dario
D
D000328:Adult; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure; D015992:Body Mass Index; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000502:physiology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control*; D007328:Insulin / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D018384:Oxidative Stress; D012016:Reference Values; D014664:Vasodilation / Q000502:physiology
D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins