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Published on: March 29, 2024
Diabetic patients without vascular complications display enhanced basal platelet activation and decreased antioxidant
Evelyne Véricel1, Caroline Januel, Martine Carreras
1Unité mixte de Recherche 585 Institut National de la Santé et de la Recherche Médicale/Institut National des Sciences Appliquées de Lyon, Institute for Multidisciplinary Biochemistry of Lipids, Villeurbanne, France. evelyn.vericel@insa-lyon.fr
Insights
Diabetic patients show increased platelet activation and oxidative stress, even without vascular complications. These findings highlight early platelet dysfunction in diabetes, contributing to vascular disease risk.
Area of Science:
- Biochemistry
- Hematology
- Endocrinology
Background:
- Vascular complications are a major cause of death in diabetic patients.
- Platelet contribution to thrombosis is known, but their role in atherosclerosis initiation is emerging.
- Diabetic platelet dysfunction may precede clinical vascular complications.
Purpose of the Study:
- To investigate basal arachidonic acid metabolism and platelet redox status in type 1 and type 2 diabetes.
- To compare these parameters in diabetic patients without vascular complications versus healthy controls.
- To understand early platelet alterations contributing to diabetic vascular disease risk.
Main Methods:
- Analysis of thromboxane B(2) and malondialdehyde levels in resting platelets.
- Measurement of platelet vitamin E levels and glutathione peroxidase activity.
- Comparison between diabetic patients (type 1 and type 2) and control groups.
Main Results:
- Significantly increased thromboxane B(2) in platelets from both type 1 (58%) and type 2 (88%) diabetic patients.
- Elevated platelet malondialdehyde in type 2 diabetes (67%).
- Reduced vitamin E levels and glutathione peroxidase activity in platelets from diabetic patients.
Conclusions:
- Platelet hyperactivation is present in well-controlled diabetic patients without complications.
- Increased oxidative stress and impaired antioxidant defenses are observed, particularly in type 2 diabetes.
- These platelet abnormalities contribute to the elevated vascular disease risk in diabetes.
Abstract:
Vascular complications are the leading causes of morbidity and mortality in diabetic patients. The contribution of platelets to thromboembolic complications is well documented, but their involvement in the initiation of the atherosclerotic process is of rising interest. Thus, the aim of the present study was to evaluate basal arachidonic acid metabolism in relation to the redox status of platelets in both type 1 and type 2 diabetic patients, in the absence of vascular complications, as compared with respective control subjects. For the first time, we show that basal thromboxane B(2), the stable catabolite of thromboxane A(2), significantly increased in resting platelets from both type 1 and type 2 diabetic patients (58 and 88%, respectively), whereas platelet malondialdehyde level was only higher in platelets from type 2 diabetic subjects (67%). On the other hand, both vitamin E levels and cytosolic glutathione peroxidase activities were significantly lower in platelets from diabetic patients as compared with respective control subjects. We conclude that platelet hyperactivation was detectable in well-controlled diabetic patients without complications. This abnormality was associated with increased oxidative stress and impaired antioxidant defense in particular in type 2 diabetic patients. These alterations contribute to the increased risk for occurrence of vascular diseases in such patients.
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