The Relationship of Oxidative Stress to Thrombotic Tendency in Type 1 Diabetic Patients with Retinopathy

Jennings, P.E.; McLaren, M.; Scott, N.; Saniabadi, A.R.; Belch, J. J. F.

doi:10.1111/j.1464-5491.1991.tb02125.x

Cited by 66 publications

(40 citation statements)

References 20 publications

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“…Moreover, non-enzymatic antioxidant elevation also has been observed in the present study after treating diabetic rats with5mg/kg and 10mg/kg of oleuropein. Vitamin Eor α-tocopherol as an essential antioxidant has been proved to be depressed when glucose level is increased in the body (26). The same results been detected in this study, it has been shown a negative correlation between serum glucose level and serum vitamin E levels of diabetic rats treated with oleuropein.…”

Section: Discussionsupporting

confidence: 89%

Antidiabetic Effect of Oleuropein from Olea europaea Leaf against Alloxan Induced Type 1 Diabetic in Rats

Qadir

Ali

Qader

2016

Braz. arch. biol. technol.

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Section: Discussionsupporting

confidence: 89%

Antidiabetic Effect of Oleuropein from Olea europaea Leaf against Alloxan Induced Type 1 Diabetic in Rats

Qadir

Ali

Qader

2016

Braz. arch. biol. technol.

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“…These results suggest a mechanism for the altered membrane fluidity and platelet hyperaggregability in diabetes. In both type 1 and type 2 diabetes, the prothrombotic tendency, which includes reduced endothelial cell production of prostacyclin and activators of fibrinolysis, together with increased platelet reactivity, is associated with increased oxidative stress and lipid peroxidation due to excess free radical activity (92,93).…”

Section: Inositol Phospholipid Turnover and Calcium Releasementioning

confidence: 99%

Platelet Dysfunction in Type 2 Diabetes

et al. 2001

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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 (PGI 2 ) 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 PGI 2 and enhances endothelial generation of PGI 2 and NO. Thus, the defects in insulin action in diabetes create a milieu of disordered platelet activity conducive to macrovascular and microvascular events. Diabetes Care 24:1476 -1485, 2001I nsulin resistance (IR) (i.e., resistance to insulin-stimulated glucose uptake) presents in a majority of individuals with type 2 diabetes; it appears to be a common precursor of both diabetes and macrovascular disease (1). IR is a multisystem disorder that is associated with multiple metabolic and cellular alterations. Factors that contribute to IR are genetics, obesity, physical inactivity, and advancing age (2). Metabolic disturbances that commonly occur in patients with IR are atherogenic dyslipidemia, hypertension, glucose intolerance, and a prothrombotic state (1,2).Atherogenic dyslipidemia is characterized by three lipoprotein abnormalities: elevated VLDL, small LDL particles, and decreased HDL cholesterol levels (the lipid triad), also named the atherogenic lipoprotein phenotype (2). This triad is the hallmark of people with diabetes and IR and appears to be an atherogenic phenotype independent of elevated levels of LDL cholesterol (2). As a corollary, most patients with IR have this phenotype even if they are not diabetic, and it may precede the development of diabetes by many years (2).Hypertension, a well-established risk factor for macrovascular events, is also associated with IR. In fact, a direct relationship between plasma insulin concentration and blood pressure has been noted (1). Although the list of multifactorial events that link hypertension and IR is growing (3), currently, the emphasis rests on the role of the endothelial cell.Hypertension is a component of the metabolic synd...

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“…Patients with type 2 diabetes have an increased production of free radicals, 1 which can inactivate nitric oxide (NO) 2 and increase diabetic complications. 3 Because endothelial dysfunction is thought to be a precursor of atherosclerosis, a promising therapeutic goal in patients with type 2 diabetes might be to reduce free radical activity.…”

mentioning

confidence: 99%

Allopurinol Normalizes Endothelial Dysfunction in Type 2 Diabetics With Mild Hypertension

et al. 2000

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Abstract-Therapeutic strategies against free radicals have mostly focused on the augmentation of antioxidant defenses (eg, vitamins C and E). A novel approach is to prevent free radical generation by the enzyme system xanthine oxidase. We examined whether the inhibition of xanthine oxidase with allopurinol can improve endothelial function in subjects with type 2 diabetes and coexisting mild hypertension compared with control subjects of a similar age. We examined 23 subjects (11 patients with type 2 diabetes and 12 healthy age-matched control subjects) in 2 parallel groups. The subjects were administered 300 mg allopurinol in a randomized, placebo-controlled study in which both therapies were administered for 1 month. Endothelial function was assessed with bilateral venous occlusion plethysmography, in which the forearm blood flow responses to intra-arterial infusions of endothelium-dependent and -independent vasodilators were measured. Allopurinol significantly increased the mean forearm blood flow response to acetylcholine by 30% (3.16Ϯ1.21 versus 2.54Ϯ0.76 mL ⅐ 100 mL Ϫ1 ⅐ min Ϫ1 allopurinol versus placebo; Pϭ0.012, 95% CI 0.14, 1.30) but did not affect the nitroprusside response in patients with type 2 diabetes. There was no significant impact on either endothelium-dependent or -independent vascular responses in age-matched control subjects. Allopurinol improved endothelial function to near-normal levels. Regarding markers of free radical activity, the level of malondialdehyde was significantly reduced (0.30Ϯ0.04 versus 0.34Ϯ0.05 mol/L for allopurinol versus placebo, Pϭ0.03) in patients with type 2 diabetes but not in control subjects. The xanthine oxidase inhibitor allopurinol improves endothelial dysfunction in patients with type 2 diabetes with mild hypertension but not in matched control subjects. In the former group, allopurinol restored endothelial function to near-normal levels.

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The Relationship of Oxidative Stress to Thrombotic Tendency in Type 1 Diabetic Patients with Retinopathy

Cited by 66 publications

References 20 publications

Antidiabetic Effect of Oleuropein from Olea europaea Leaf against Alloxan Induced Type 1 Diabetic in Rats

Antidiabetic Effect of Oleuropein from Olea europaea Leaf against Alloxan Induced Type 1 Diabetic in Rats

Platelet Dysfunction in Type 2 Diabetes

Allopurinol Normalizes Endothelial Dysfunction in Type 2 Diabetics With Mild Hypertension

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