Background: Reactive oxygen species generated by hyperglycaemia modify structure and function of lipids, proteins and other molecules taking part in chronic vascular changes in diabetes mellitus (DM). Low activity of scavenger enzymes has been observed in patients with DM. Protective role of scavenger enzymes may be deteriorated by oxidative stress. This study was undertaken to investigate the association between gene polymorphisms of selected antioxidant enzymes and vascular complications of DM.
The relationship between arterial hypertension and insu lin resistance has long been established. We used primary hyperal dosteronism as a model of the relationship between secondary hy pertension and insulin sensitivity. Our group consisted of 9 patients with arterial hypertension caused by primary hyperaldosteronism. Five of these patients with aldosterone producing adenoma were operated on and four patients with idiopathic hyperaldosteronism were treated with spironolactone. Hyperinsulinaemie euglycaemic clamp technique was performed before and at least 6 months fol lowing the treatment to evaluate the insulin action. Significantly lower glucose disposal rate (M), insulin sensitivity index (M/I) and decreased metabolic clearance rale of glucose (MCR (i ) were found in patients before treatment as compared to healthy controls. In both treated groups the blood pressure and plasma potassium con centrations returned to normal values, whereas plasma aldosterone levels were normalised only after surgical removal of the adenoma. Significantly improved insulin action (M/I: 30.2 ± 5.9 vs. 51.4 ± 12.2 umol.kg" '.min 1 per mU.l" 1 X 100, p = 0.017) was observed in patients after operation of aldosterone producing adenoma. In contrast, spironolactone treatment of patients with idiopathic hyp eraldosteronism did not significantly influence insulin action (M/I: 24.5 ± 7.3 vs. 18.7 ± 7.6 umol.kg-'.rnin-' per mU.l 1 x 100, p = 0.198). Since plasma aldosterone concentrations have been normal ised only in patients after removal of the adenoma whereas they remained increased in spironolactone treated group, we suppose that aldosterone itself could play a role in the development of im paired insulin action. Downloaded by: Collections and Technical Services Department. Copyrighted material. G. Sindelka et al., Insulin action in primary hyperaldosteronism Torlone E, Rambotti AM, Perriello G, Botta G, Santeusanio F, Brunetti P, Bolli GB: ACE-inhibition increases hepatic and extrahepatic sensitivity to insulin in patients with type 2 (non-insu lin-dependent) diabetes mellitus and arterial hypertension. Diabetologia 34: 119-125, 1991 Tylor SI: Lilly lecture: Molecular mechanisms of insulin resistance. Lessons from patients with mutations in the insulin-receptor gene. Diabetes 41: 1473-1490, 1992 Widimsky J, Skrha J, Sindelka G, Hilgertova J: Is insulin resistance in primary hyperaldosteronism modifiable by treatment? J Hypert 16, Suppl SI48, 1998 Yajnik CS, Naik SS, Bhat DS, Joshi VM, Shelgikar KM, Alberti KGMM, Hockaday TDR: The relationship between obesity, 25 plasma immunoreactive insulin concentration and blood pres sure in newly diagnosed Indian type 2 diabetic patients. Diab Med 10: 146-151, 1993 Zemel MB: Insulin resistance, obesity and hypertension: an over view.
We conclude that initiation of metformin treatment in type 2 diabetic patients is associated with improved diabetes control as well as with activation of oxidative stress together with antioxidant system. The atherogenic process measured by biochemical indicators is diminished in parallel. Our results show that in short-term metformin administration in type 2 diabetes promotes endothelium effects associated with a complex of metabolic changes.
This study attempted to verify the existence of a relationship between oxidative stress documented by malondialdehyde (MDA) and superoxide dismutase (SOD) and fibrinolysis analysed by tissue plasminogen activator (tPA) and its inhibitor (PAI‐1) in diabetes mellitus. Forty‐seven patients with Type 1 (n = 27) and Type 2 (n = 20) diabetes were examined together with 20 non‐diabetic controls. The following were analysed: plasma MDA concentration, SOD activity in erythrocytes, tPA activity and antigen, PAI‐1 activity and antigen, fasting blood glucose, fructosamine, glycated haemoglobin (HbAlc), and urine albumin. SOD activity was decreased in patients with diabetes. This contrasted with an increased plasma MDA concentration especially in Type 2 diabetes as compared with Type 1 or healthy persons (p < 0.001). tPA activity was increased in both groups of patients with diabetes as compared to healthy persons (p < 0.001), PAI‐1 activity was higher in Type 2 diabetes with vascular changes than in the remaining subgroups (p < 0.001). Multivariate analysis revealed a significant positive relationship between plasma MDA concentrations and PAI‐1 antigen (r = 0.53, p < 0.001) and a negative relationship between SOD and tPA activities (r = −0.53, p < 0.01). We conclude that oxidative stress may modulate fibrinolytic properties in diabetes mellitus.
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