Biomedical subjects

H Hatemi

Publications and source records attributed to H Hatemi.

At least 37 records · Page 2Linked to original sources

PubMed1997

Calcium, magnesium, and zinc status in experimental hyperthyroidism.

In this study, experimental hyperthyroidism was established and used to investigate possible alterations in the calcium (Ca), magnesium (Mg), and zinc (Zn) homeostasis by assessing their concentrations in plasma and erythrocytes. In the L-thyroxine-induced hyperthyroidism condition, the experimental animals show a significant decrease in erythrocyte Ca, Mg, and Zn concentrations, and a significant decrease in plasma Mg concentration. Significant positive correlations were found for Mg and Zn both in plasma and in erythrocytes. The results suggest that the homeostasis of Ca, Mg, and Zn is altered during experimental hyperthyroidism.

Animals↗

PubMed1997

Calcium, magnesium, and zinc status in experimental hypothyroidism.

In this study, experimental hypothyroidism was established and used to investigate possible alterations in the calcium, magnesium, and zinc homeostasis by assessing their concentration in plasma and erythrocytes. Hypothyroidism was induced by administration of methimazole an iodine blocker at a dose of 75 mg/100 g food for 3 wk. In the methimazole-induced hypothyroid state, the experimental animals showed a significant decrease in plasma zinc concentration, whereas a significant increase in plasma magnesium concentration occurred. No change was observed in plasma calcium concentration. The erythrocyte zinc and calcium concentrations were found to be increased, whereas magnesium concentration decreased. Erythrocyte magnesium concentration showed a significant positive correlation with T4 values. The study provides evidence for marked alterations in homeostatis of zinc, magnesium, and calcium.

Animals↗

PubMed1997

The erythrocyte glutathione levels during oral glucose tolerance test.

Erythrocytes glutathione (GSH) levels were measured in erythrocytes from 33 subjects, at baseline and after 2-hour glucose loading in order to investigate the effect of glucose ingestion on the erythrocyte GSH. According to the World Health Organisation criteria 18 subjects had normal glucose tolerance (NGT)(mean age 48 +/- 10 years, 10 women, 8 men), 15 subjects had impaired glucose tolerance (IGT)(mean age 52 +/- 8 years, 9 women, 6 men). After 12-hour fasting, erythrocyte GSH levels were 40.5 +/- 8.06 and 39.27 +/- 10.26 mg/dl hemolisate in subjects with NGT and IGT, respectively (p = N.S). After 2-hour glucose loading, erythrocyte GSH levels decreased to 36.01 +/- 9.4 (p < 0.05) and 32.36 +/- 5.7 (p < 0.005) in subjects with NGT and IGT, respectively. The decrease in erythrocyte GSH levels in subjects with IGT was greater than in NGT individuals (p < 0.001). There was negative correlation between glucose, insulin, C-peptide, and erythrocyte GSH levels after glucose loading (p < 0.005). Our results suggest that glucose loading induce an oxidative stress in all subjects but this oxidative stress is greater in subjects with IGT than with NGT.

Blood Glucose↗

PubMed1997

Cerebellar syndrome due to hypoparathyroidism.

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Cerebellar Diseases↗

PubMed1997

The effect of iron supplementation on GSH levels, GSH-Px, and SOD activities of erythrocytes in L-thyroxine administration.

Our aim was to study the effect of iron supplementation on the following aspects of erythrocyte metabolism in experimental hyperthyroidism: glutathione (GSH) levels, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities. Hyperthyroidism induced by L-thyroxine administrations significantly raised erythrocyte GSH, GSH-Px and SOD levels of the rats (P < 0.001). Likewise, we observed that iron supplementation induced significant rises in erythrocyte GSH, GSH-Px and SOD levels (P < 0.001) as compared with the control group. The erythrocyte GSH, GSH-Px and SOD levels of hyperthyroidism-induced iron-supplemented animals were significantly higher when compared with either the iron-supplemented group (P < 0.001) or the only L-thyroxine-administered hyperthyroid group (P < 0.001, P < 0.05, P < 0.01, respectively). The results of this study show that L-thyroxine administration and/or iron supplementation increases GSH, GSH-Px and SOD levels of erythrocytes.

Animals↗

PubMed1996

Antioxidant status in experimental hyperthyroidism: effect of vitamin E supplementation.

Free radical-mediated oxidative stress has been implicated in the genesis and exacerbation of degenerative diseases. In view of the role of oxidative processes in hyperthyroidism, in this study, we investigated the antioxidant status of erythrocytes in experimental hyperthyroidism and the effect of vitamin E supplementation on defense systems. Our findings of significantly increased T4 and T3 and undetectable TSH values in thyroxine administered rats confirmed the establishment of hyperthyroidism. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH) values were found to be significantly increased in hyperthyroid rats in comparison to the control group. Vitamin E supplementation to hyperthyroid rats induced a significant decrease in GSH-Px activity and a significant increase in GSH level. These findings show that hyperthyroidism increases the components of the antioxidant system in the erythrocytes. Furthermore, vitamin E supplementation reduces the burden of oxidative stress in hyperthyroidism.

Animals↗

PubMed1996

Lipid peroxidation and vitamin E supplementation in experimental hyperthyroidism.

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Animals↗

PubMed1995

The effect of metformin on insulin receptors and lipid peroxidation in alloxan and streptozotocin induced diabetes.

Biguanides are used for the treatment of non-insulin dependent diabetes mellitus but there is no evidence for an improving action of biguanide on the enhancement of peripheral glucose disposal in type 1 diabetes. It is known that biguanide agents reduce the oxidation of free fatty acids. Using alloxan and streptozotocin (STZ) induced diabetic rats as a model for type 1 diabetes mellitus, we measured insulin binding capacity and plasma lipid peroxidation levels before and after metformin induction. There was a significant increase in insulin binding capacity and lipid peroxidation levels in alloxan and STZ diabetes compared to controls. We examined the effect of metformin on alloxan and STZ-induced diabetic rats. In alloxan-induced diabetes metformin (Met) treatment led to an increase in insulin receptor number in liver plasma membranes (before Met: 46.50 +/- 2.69, after Met: 76.00 +/- 3.39 fmol/mg, p < 0.001) and a decrease in plasma lipid peroxidation levels compared to the non-treated group (before Met: 1.85 +/- 0.53, after Met: 1.10 +/- 0.09 nmol MDA/ml, p < 0.05). In STZ-induced diabetic rats metformin treatment did not change the lipid peroxidation levels (before Met: 1.26 +/- 0.31, after Met: 1.38 +/- 0.44 nmol MDA/ml, p > 0.05) whereas it did increase the receptor numbers (before Met: 41.60 +/- 4.33, after Met: 63.40 +/- 8.64 fmol/mg, p < 0.002).

Alloxan↗

PubMed1993