Platelet Dysfunction in Type 2 Diabetes

DOI PDF 被引用文献12件
  • Aaron I. Vinik
    Department of Medicine and Pathology/Anatomy/Neurobiology, the Strelitz Diabetes Research Institutes, Eastern Virginia Medical School, Norfolk, Virginia
  • Tomris Erbas
    Department of Medicine and Pathology/Anatomy/Neurobiology, the Strelitz Diabetes Research Institutes, Eastern Virginia Medical School, Norfolk, Virginia
  • Tae Sun Park
    Department of Medicine and Pathology/Anatomy/Neurobiology, the Strelitz Diabetes Research Institutes, Eastern Virginia Medical School, Norfolk, Virginia
  • Roger Nolan
    Cato Research Ltd., Research Triangle Park, North Carolina
  • Gary L. Pittenger
    Department of Medicine and Pathology/Anatomy/Neurobiology, the Strelitz Diabetes Research Institutes, Eastern Virginia Medical School, Norfolk, Virginia

抄録

<jats:p>Insulin resistance is a uniform finding in type 2 diabetes, as are abnormalities in the microvascular and macrovascular circulations. These complications are associated with dysfunction of platelets and the neurovascular unit. Platelets are essential for hemostasis, and knowledge of their function is basic to understanding the pathophysiology of vascular disease in diabetes. Intact healthy vascular endothelium is central to the normal functioning of smooth muscle contractility as well as its normal interaction with platelets. What is not clear is the role of hyperglycemia in the functional and organic microvascular deficiencies and platelet hyperactivity in individuals with diabetes. The entire coagulation cascade is dysfunctional in diabetes. Increased levels of fibrinogen and plasminogen activator inhibitor 1 favor both thrombosis and defective dissolution of clots once formed. Platelets in type 2 diabetic individuals adhere to vascular endothelium and aggregate more readily than those in healthy people. Loss of sensitivity to the normal restraints exercised by prostacyclin (PGI2) and nitric oxide (NO) generated by the vascular endothelium presents as the major defect in platelet function. Insulin is a natural antagonist of platelet hyperactivity. It sensitizes the platelet to PGI2 and enhances endothelial generation of PGI2 and NO. Thus, the defects in insulin action in diabetes create a milieu of disordered platelet activity conducive to macrovascular and microvascular events.</jats:p>

収録刊行物

  • Diabetes Care

    Diabetes Care 24 (8), 1476-1485, 2001-08-01

    American Diabetes Association

被引用文献 (12)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ