Objectives: To measure plasma adiponectin concentrations in patients with type 2 diabetes and to investigate any association with the severity of diabetic retinopathy, because adiponectin seems to be an important modulator for metabolic and vascular diseases. Methods: Seventy-four patients (mean age 46.8^5.1 years; body mass index (BMI), 26.8^2.10 kg/m 2 ) and 54 healthy volunteers (mean age 46.8^5.4 years; BMI 26.47^2.33 kg/m 2 ) were included. Results: Adiponectin concentrations in the patients were significantly lower than those in controls (4.71^2.11 mg/ml for patients, n ¼ 74; 15.95^3.72 mg/ml for controls, n ¼ 54; P , 0.001). In the patients group there was a significant negative correlation between adiponectin and homeostasis model assessment index (r ¼ 2 0.318, P ¼ 0.006 respectively). Plasma adiponectin concentrations in patients with proliferative diabetic retinopathy (n ¼ 20; 3.16^1.83 mg/ml) or non-proliferative diabetic retinopathy (n ¼ 24; 3.97^1.47 mg/ml, P ¼ 0.014) were significantly lower than those in patients without diabetic retinopathy (n ¼ 30; 6.30^1.57 mg/ml, P ¼ 0.001). When the presence of diabetes was defined as the final variable in the conditional logistic regression model with the adiponectin concentration as the continuous variable, adiponectin was significantly involved in the model.
Conclusion:The results show that adiponectin concentrations are lower in patients with type 2 diabetes and that the concentrations are associated with the severity of diabetic retinopathy. Our findings suggest that adiponectin may take part in the pathogenesis of diabetic retinopathy.
Providing patients with comprehensive knowledge about statins, even in patients, who were already on statin therapy, seems not only to improve adherence but also increase the percentage of those reaching targets.
Objective: Previous studies have demonstrated that low plasma adiponectin concentrations are associated with essential hypertension. It has also recently been shown that adiponectin plays an essential role in the modulation of angiogenesis. These data led us to hypothesize that adiponectin might contribute to end-organ damage in hypertension. Methods: In the present study we have evaluated the relationship between plasma adiponectin concentrations and hypertensive retinopathy. One hundred and ten patients newly diagnosed with essential hypertension (EHT) (mean age, 46.79^5.0 years; body mass index (BMI), 26.47^2.23 kg/m 2 ; male/female ratio, 58/52) and 57 healthy normotensive control subjects (NT) (mean age, 46.84^5.4 years; BMI, 26.66^2.65 kg/m 2 ; male/female ratio, 33/24) were enrolled. Results: Plasma adiponectin levels were significantly lower in EHT than in NT (P , 0.001). In addition, adiponectin concentrations were strongly correlated with systolic and diastolic blood pressures in EHT (r ¼ 2 0.757, P , 0.001; r ¼ 20.761, P , 0.001) while there was no correlation in the NT group. Plasma adiponectin in patients with grade 0 hypertensive retinopathy (n ¼ 52) was significantly higher than that of the patients with grade 1 (n ¼ 30) and 2 (n ¼ 28) hypertensive retinopathy (P , 0.001 for each). Plasma adiponectin in patients with grade 0 hypertensive retinopathy was also significantly lower than that in the NT group (P , 0.001). The estimated threshold of plasma adiponectin concentration for hypertensive retinopathy was 17 mg/ml. This critical adiponectin level served largely to separate patients with retinopathy from those without. Conclusion: Our results have shown that plasma adiponectin concentrations decrease progressively with higher grades of hypertensive retinopathy even after correction for other atherogenic risk factors, suggesting that a critical adiponectin level is needed for the development of retinopathy. 152 233-240
European Journal of Endocrinology
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