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Increased biosynthesis of thromboxane A 2 by diabetic platelets
Author(s) -
ZIBOH VINCENT A.,
MARUTA HIROYUKI,
LORD JONATHAN,
CAGLE WILLIAM D.,
LUCKY WILLIAM
Publication year - 1979
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1979.tb00927.x
Subject(s) - platelet , medicine , thromboxane , arachidonic acid , endocrinology , thromboxane a2 , biosynthesis , thromboxane b2 , thromboxane a synthase , chemistry , biochemistry , enzyme
. Because ADP has been reported to produce a secondary wave of platelet aggregation in diabetic subjects, and since ADP is known to enhance normal platelet biosynthesis of pro‐aggregating thromboxane A 2 , we tested whether or not the reported increased sensitivity of diabetic platelets to ADP may also result in increased platelet biosynthesis of thromboxane A 2 . To test this hypothesis, 14 C‐arachidonic acid ( 14 C‐AA) was incubated in vitro with washed human platelets' in the presence or absence of ADP. These studies included platelets isolated from thirty normal volunteers, twenty‐six diabetic subjects with and without known vascular complications, eighteen non‐diabetic pregnant females and fourteen pregnancy‐induced diabetic females. Data from these studies demonstrated: (i) a significant increase in the capability of diabetic platelets in response to ADP to biosynthesize thromboxane A 2 from arachidonic acid when compared to platelets from normal controls ( P < 0.001); (ii) a significant increase in thromboxane A 2 biosynthesis by platelets from pregnancy‐induced diabetic subjects over nondiabetic pregnant females ( P < 0.001); (iii) a two‐fold increase in thromboxane A 2 biosynthesis by platelets from diabetic subjects with vascular complications when compared to those without vascular complications. Although our data also showed approximately a twofold increase in thromboxane A 2 biosynthesis by platelets from diabetic subjects with greater than 10 years of the disease when compared to diabetic subjects with less than 10 years, these latter results were, however, not statistically significant. Results from these studies suggest that a relationship may exist between the markedly increased ADP‐induced platelet aggregation in diabetes mellitus and the vascular complications associated with this disease. Whether or not increased capacity of the diabetic platelet to biosynthesize pro‐aggregating thromboxane A 2 in response to ADP or other pro‐aggregating agents is per se a triggering factor in occlusive vascular diseases reported in diabetic subjects must await further studies.