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Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1187-1193
Published online before print May 16, 2002, doi: 10.1161/01.ATV.0000021759.08060.63
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1187.)
© 2002 American Heart Association, Inc.


Atherosclerosis and Lipoproteins

Monocyte and Neutrophil Adhesion Molecule Expression During Acute Hyperglycemia and After Antioxidant Treatment in Type 2 Diabetes and Control Patients

M.J. Sampson; I.R. Davies; J.C. Brown; K. Ivory; D.A. Hughes

From Bertram Diabetes Research Unit (M.J.S., I.R.D.), Department of Diabetes & Endocrinology, Norfolk and Norwich University Hospital NHS Trust, and the Institute of Food Research (I.R.D., J.C.B., K.I, D.A.H.), Norwich Research Park, Colney, Norwich, UK.

Correspondence to M.J. Sampson, Department of Endocrinology and Diabetes, Norfolk and Norwich Hospital, Brunswick Road, Norwich NR1 3SR UK. E-mail mike.sampson{at}norfolk-norwich.thenhs.com

Objective We hypothesized that acute hyperglycemia (an independent cardiovascular risk factor) increases the expression of proatherogenic leukocyte adhesion molecule in type 2 diabetes and controls and that the expression of these adhesion molecules would be antioxidant sensitive.

Methods and Results Twenty-three type 2 diabetes patients and 13 control patients underwent two oral glucose tolerance tests 14 days apart and took placebo or 800 IU daily of oral alpha tocopherol between tests. Monocyte and neutrophil expression of adhesion molecules Mac-1, LFA-1 and 3, ICAM-1, and VLA-4 were measured at 0, 120, and 240 minutes by using laser flow cytometry. Baseline adhesion molecule expression did not differ between groups, but there was a rapid, highly significant increase (P<0.0001) in the intensity of monocyte Mac-1 expression after a glucose load in both groups. Alpha-tocopherol supplementation reduced only Mac-1 expression in the diabetes group (P=0.03).

Conclusions Acute glycemic excursions of any degree cause highly significant, rapid increases in monocyte Mac-1 expression in type 2 diabetes patients and controls. Mac-1 mediates leukocyte vascular infiltration and is prothrombotic. These data suggest a mechanism for the link between glycemic excursions and increased vascular event rates.


Key Words: type 2 diabetes • monocyte • adhesion molecule • hyperglycemia • antioxidants




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