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        Angiotensin-I converting enzyme gene polymorphism in Turkish type 2 diabetic patients

        H . Arzu Ergen,Husrev Hatemi,Bedia Agachan,Hakan Camlica,Turgay Isbir 생화학분자생물학회 2004 Experimental and molecular medicine Vol.36 No.4

        Non-insulin dependent diabetes melitus is often associated with some complications such as nephropathy, retinopathy and neuropathy. Genes of the renin angiotensin system are potential candidate genes for diabetic complications. We investigated the relationship betwen angio-phism in type 2 diabetic patients with and with-out diabetic nephropathy. Seventy five patients (25 type 2 diabetic patients with nephropathy, 50 type 2 diabetic patients without nephropathy) and 37 healthy controls were studied. Gene polymorphism of ACE was determined by PCR (polymerase chain reaction) amplification using allele-spesific primers. The frequencies of ACE D, ID and II genoypes among the patients with type 2 diabetic patients were found 48%, 42%, 10% whereas in control subjects, 27%, 60%, ing DD genotype without nephropathy increased 1.77 fold than control subjects (P< 0.05). There is no significant corelation between diabetic nephropathy and ACE gene polymorphism. But we found that ACE DD genotype increased significantly in type 2 diabetic patients com-pared to control subjects (P< 0.05).

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        Iron Supplementation in Experimental Hyperthyroidism: Effects on Oxidative Stress in Skeletal Muscle Tissue

        Hakki Oktay Seymen,Sabiha Civelek,Arzu Seven,Gunnur Yigit,Husrev Hatemi,Gulden Burcak 연세대학교의과대학 2004 Yonsei medical journal Vol.45 No.SUP

        This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.

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