Effects of nonenzymatic glycosylation on antithrombin III.

概要

論文の詳細を見る
Antithrombin III (AT III) is one of the most potent serine protease inhibitors, and the functional abnormalities of this inhibitor have been proved to be the pathogenesis of thromboembolism in the traits of congenital abnormal AT III. These abnormalities are also considered to be caused by some environmental factors. In this paper we have evaluated the possibility of glucose to reduce AT III activity and the contribution of impaired AT III activity to hypercoagulable state in diabetic patients.When human citrated plasma was aseptically incubated with glucose (0-2.0M) at 37°C for up to seven days, heparin cofactor activity of AT III gradually decreased, depending on the added glucose concentration or incubation period. Moreover AT III or these samples showed the increase of slow moving peak on modified crossed immunoelectrophoresis, and the increase of the bands with lower pis (isoelectric points) which was accompanied by the decrease of other hands on agarose gel isoelectric focusing.In plasma of diabetic patients, a significant inversed correlation exists between the ratio of heparin cofactor activity to antithrombin III antigen and the levels of hemoglobin A1c.Glycosylated AT III was considered to be responsible for the functional and constitutional abnormalities of plasma AT III and it was suspected to be important as the pathogenesis of diabetic microangiopathy in diabetes mellitus.
一般社団法人日本血栓止血学会の論文