Type 2 diabetes mellitus is associated with impaired endothelial function and increased levels of TNF-alpha, IL-6 and sVCAM-1, especially in patients with DM and CAD. Vitamin C significantly increased forearm vasodilatory response to reactive hyperaemia only in patients with combined DM and CAD.
FACC 1OBJECTIVE -To examine the effect of vitamin C on forearm vasodilatory response to reactive hyperemia and on plasma level of plasminogen activator inhibitor 1 (PAI-1), von Willebrand factor (vWF), tissue plasminogen activator (tPA), antithrombin III (ATIII), proteins C and S, and factors V (fV) and VII (fVII) in patients with both type 2 diabetes and CAD.RESEARCH DESIGN AND METHODS -A total of 39 patients with type 2 diabetes and CAD were divided into two groups and received vitamin C (2 g/day) or no antioxidant for 4 weeks. Forearm blood flow was determined using venous occlusion gauge-strain plethysmography at baseline and after treatment. Forearm vasodilatory response to reactive hyperemia (RH%) or nitrate (NTG%) was defined as the percent change of flow from baseline to the maximum flow during reactive hyperemia or after administration of nitrate, respectively. Biochemical markers were determined by enzyme-linked immunosorbent assay (ELISA) or other standard methods.RESULTS -RH% was significantly increased after treatment with vitamin C (from 62.4 Ϯ 7.2 to 83.1 Ϯ 9.3%, P ϭ 0.024) but remained unaffected in the control group. Vitamin C decreased plasma levels of fV (from 143 Ϯ 5.4 to 123 Ϯ 6.03%, P ϭ 0.038), vWF (from 133.5 Ϯ 14.5 to 109.5 Ϯ 11.4%, P ϭ 0.016), and tPA (from 12.3 Ϯ 0.99 to 8.40 Ϯ 0.60 ng/ml, P ϭ 0.001), whereas these levels remained unaffected in the control group. The changes in RH%, vWF, and tPA were significantly greater (P ϭ 0.028, 0.036, and 0.007, respectively) in the vitamin C-treated group than in the control group. Levels of ATIII, proteins S and C, fVII, and PAI-1 remained unchanged in all groups.CONCLUSIONS -Short-term treatment with high doses of vitamin C improved RH% and decreased plasma levels of tPA and vWF in patients with type 2 diabetes and CAD. Diabetes Care 26:2749 -2753, 2003I n the last decade, our knowledge of diabetes has evolved and new disorders such as oxidative stress (1), endothelial dysfunction (1,2), and impaired fibrinolytic activity (3) have been suggested to explain, at least in part, the pathophysiology of the observed coronary atherothrombosis. Each of these abnormalities, which play important roles in the development and progression of cardiovascular disease, also provides new targets for treatment.It has been shown recently that patients with diabetes have lower serum levels of vitamin C than nondiabetic subjects, and this is believed to be an important factor contributing to the increase of oxidative stress status and endothelial dysfunction in diabetes (4). The underlying mechanisms of vitamin C deficiency in diabetes are unclear. The reduced renal reabsorption of vitamin C induced by hyperglycemia, the competition between glucose and vitamin C for the uptake into certain cells and tissues, and a possible secondary depletion due to increased oxidative stress have been proposed (4). However, the role of vitamin C treatment in patients with type 2 diabetes with or without advanced atherosclerosis is controversial (2). Antioxidant treatment depresses ...
BackgroundExcept for the established risk factors, presence of target organ damage has an important role in the treatment of hypertensive subjects. The aim of the present study was to estimate the prevalence of target organ damage in primary care subjects.MethodsThis multi-centre, cross-sectional survey of 115 primary care physicians recruited 1095 consecutive subjects with hypertension: 611 men (55.8%); and 484 women (44.2%). A detailed history for the presence of cardiovascular disease and a thorough clinical examination was performed to each subject.ResultsOf the total study population, 44.5% (n = 487) had target organ damage (33.0% had left ventricular hypertrophy, 21.8% increased carotid intima media thickness, 11.0% elevated plasma creatinine levels and 14.6% microalbuminuria). Target organ damage was more prevalent in males than in females (P = 0.05). In addition, males had more often increased carotid intima media thickness than females (P = 0.009). On the contrary, females had more often microalbuminuria (P = 0.06) than males. No differences were observed between the two genders regarding left ventricular hypertrophy (P = 0.35) and elevated plasma creatinine levels (P = 0.21). Logistic regression analysis showed associations between target organ damage and dyslipidemia (P < 0.001), presence of metabolic syndrome (P = 0.005), diabetes (P < 0.001) and coronary artery disease (P < 0.001).ConclusionA significant proportion of hypertensive subjects in primary care had documented associated target organ damage, with left ventricular hypertrophy being the most prevalent target organ damage.
Role of tumor necrosis factor-␣, leptin, and white blood cell count in betel nut chewing-related metabolic derangements A reca nut (Areca catechu)/betel quid (BQ) is said to be the fourth most commonly used psychoactive substance in the world and is chewed regularly by at least 10% of the world's population (1). High prevalences of BQ chewing were observed especially in South and Southeast Asia (1). High prevalences of insulin resistance and metabolic syndrome were also observed in this area (2). Specific areca alkaloids act as competitive inhibitors of ␥-aminobutyric acid receptors in the brain, cardiovascular system, and pancreas, which may promote one's appetite or altered insulin secretion (3). Moreover, BQ components have recently been shown to induce keratinocytes to secrete tumor necrosis factor-␣ (TNF-␣) and interleukin-6, as well as induce reactive oxygen species and activate nuclear factor-B expression (4), which may potentially provoke chronic inflammation. Recently, we confirmed that BQ chewing was associated with a higher risk of type 2 diabetes and central obesity in Taiwanese men (5). The detrimental effects of BQ chewing on selected components of the metabolic syndrome, and the induction of inflammatory cytokines and factors, raise the possibility that BQ chewing may increase the risk of metabolic syndrome.In this study, a total of 1,466 aboriginal subjects of Southern Taiwan, 30 -95 years of age, were enrolled. Metabolic syndrome was defined according to the National Cholesterol Education Program Adult Treatment Panel III definition. The age-adjusted prevalence of metabolic syndrome in the aborigines studied was 41.1% in men and 42.4% in women. BQchewing subjects had significantly higher prevalences of central obesity, hypertriglyceridemia, dysglycemia, and metabolic syndrome than those of nonchewers. Peripheral leukocyte count also significantly increased in chewers of both sexes, with plasma TNF-␣ level increased in men and plasma leptin level elevated in women. All were parallel to the number of components of the metabolic syndrome. Multiple logistic regression modeling adjusted for age, educational level, socioeconomic level, exercise, drinking, and smoking status showed that BQ chewing is an independent risk factor for the metabolic syndrome. The adjusted OR (95% CI) for male BQ chewers was 1.92 (1.15-3.27) and that of female chewers was 1.60 (1.03-2.50). The study shows that chronic BQ chewing is an independent contributor of metabolic syndrome. TNF-␣, leptin, and leukocyte count are involved in BQ chewing-related metabolic derangements.
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