Comparison of therapeutic effects of L-Thyroxin, apelin and a combination of both on antioxidant enzymes in the heart of PTU-induced hypothyroid rats

Atherosclerosis is one of the common disorders among hypothyroidism, which, increased the risk of cardiovascular diseases. Reactive oxygen species are associated with atherosclerosis development. Antioxidant defense systems are the scavenger for free radicals. Apelin is an endogenous ligand for the APJ receptor (apelin receptor) that exists in most tissues, acts as an adiponectin. It has been identified that apelin administration, improve the antioxidant capacity (TAC). Therefore, this study was conducted to assess, therapeutic effects of apelin, T4 (L-Thyroxin) or both on antioxidant capacity in 6-propyl-2-thiouracil (PTU)-induced hypothyroid rats. Forty male Wistar rats were randomly assigned into five groups: C: control group; P group (hypothyroid): PTU (0.05 %) administration for six weeks; P+A, P+T and P+A+T groups: after 4 weeks of PTU administration, animals treated with Apelin (200 μg/kg/day, ip) T4 (0.02 µg/g/day, gavage) and apelin+T4; for two weeks respectively accompanied by PTU administration. Aplein administration in P+A group and P+A+T group had beneficial effect to lowering of malondialdehyde (MDA) content as compared to hypothyroid group (8.52±0.64 and 8.53±1 vs. 13.67±1.64 nmol/g tissue, P<0.05) and also had increasing effect on Superoxide dismutase (SOD) and glutathion peroxidase (GPx) activity and the total antioxidant capacity (TAC) content compared to the hypothyroid group. This study showed that apelin was able to improve the oxidant-antioxidant balance in the heart tissue of the hypothyroid rats by elevating of antioxidant enzyme activity.

Small ubiquitin-like modifier 4 M55V polymorphism is not associated with diabetic nephropathy in Iranian type 2 diabetes patients.

INTRODUCTION: We studied the impact of small ubiquitin-like modifier 4 (SUMO4) M55V polymorphism on susceptibility to diabetic nephropathy in Iranian type 2 diabetes patients. MATERIALS AND METHODS: The patient group consisted of 50 Iranian type 2 diabetes patients with nephropathy, and the control group consisted of 50 Iranian type 2 diabetes patients without nephropathy. Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism method for the M55V. RESULTS: The frequency of SUMO4 AA, AG, and GG genotypes were 23%, 18%, and 9% in the patient group and 10%, 22%, and 18% in the control group. There was no significant difference in frequency of SUMO4 genotypes in patients compared to controls. CONCLUSION: These findings indicate that SUMO4 M55V polymorphism is not associated with diabetic nephropathy in Iranian type 2 diabetes patients.

Analysis of loss of heterozygsity effect on thyroid tumor with oxyphilia cell locus in familial non medullary thyroid carcinoma in Iranian families.

Material and Methods: 22 nuclear families (78 persons including 12 patients) with papillary and follicular tumors were selected in a period of six months from Milad hospital. Five microsatellite markers (D19S413, D19S391, D19S916, D19S568, D19S865) on 19p13.2 were selected for genetic analysis. Genomic DNAs was extracted; PCR and polyacrylamide gel electrophoresis method were used for variation detection. Results: The results show that 5.4% of the follicular carcinomas and 17.9% of the papillary carcinomas presented LOH at recognition sites. LOH of Papillary carcinoma detected about 13.9% and follicular carcinoma 7.2% in this study. The frequency of informative cases was not similar for each marker: D19S413 (41.1%)[1], D19S391 (12.5%), D19S916 (10.7%), D19S568 (1.8%) and D19S865 (3.6%). Loss of hetrozygosity in D19S413 predicts the relation between variation in this region and the disease. Discussion: Our findings showed an average of 13.9% LOH in FNMTC cases. Among the five major microsatellites, D19S413 was the most informative for LOH analysis of FNMTC.

TaqI B1/B2 and -629A/C cholesteryl ester transfer protein (CETP) gene polymorphisms and their association with CETP activity and high-density lipoprotein cholesterol levels in a Tehranian population. Part of the Tehran Lipid and Glucose Study (TLGS)

We examined the cholesteryl ester transfer protein (CETP) gene TaqI intron 1 B1/B2 polymorphism and the -629A/C CETP promoter polymorphism in respect to high-density lipoprotein cholesterol (HDL-C) in a healthy Iranian population taken from the Tehran Lipid and Glucose Study (TLGS). The relationship between CETP activity and HDL-C level was also determined along with body mass index, blood pressure and tobacco smoking status. PCR-RFLP used to amplify a segment of the CETP intron 1 TaqI (B2/B1) polymorphism from 1021 individuals and we selected 345 individuals from the lowest, middle and highest HDL-C deciles and investigated the -629A/C polymorphism. We also evaluated the CETP activity of 103 of these individuals, each with at least one homozygous allele. The presence of the TaqI B2 and -629A/C A alleles were significantly associated with increased HDL-C levels (B2B2 = 1.19 ± 0.31 mmolL-1 vs. B1B1 = 1.01 ± 0.2 mmol L-1 for p < 0.001; AA = 1.15 ± 0.41 mmol L-1 vs. CC = 0.95 ± 0.28 mmol L-1 for p < 0.001) and decreased the CETP activity (B1B1 = 67.8 ± 8.9 pmol L-1 vs. B2B2 = 62.6 ± 9.6 pmol L-1 for p < 0.01; CC = 68.6 ± 8.4 pmol L-1 vs. AA = 62.7 ± 9.7 pmol L-1 for p < 0.002). The frequencies were 0.382 for the TaqI B2 allele and 0.462 for the -629A/C A allele, with linkage disequilibrium analysis giving D = 0.0965 and D' = 0.4695. We demonstrated that the TaqI B1 and B2 alleles and the -629A/C A and C alleles were in linkage disequilibrium in our population and that there was a significant association between the B2 and A alleles and high HDL-C levels and low CETP activity. Linkage disequilibrium between the TaqI A and B2 alleles also detected.

Insulin resistance in chronic hepatitis B and C.

AIM: To determine whether insulin resistance occurs in patients with chronic hepatitis B (CHB) and chronic hepatitis C (CHC) and its relationship with the presence of liver fibrosis and steatosis. METHODS: Untreated patients with CHC (n=60) or CHB (n=40), similar in age, gender, body mass index and waist-hip ratio, were studied. Relationship between anthropometric, biochemical (fasting serum insulin, C-peptide, ferritin, iron, TNF-alpha, cholesterol, triglyceride, bilirubin, hemoglobin and platelet concentrations) and liver biopsy (43 CHC and 20 CHB patients) findings was investigated by insulin resistance determined via the homeostasis model assessment (HOMA-IR). RESULTS: The mean fasting serum insulin was 14.9 (11.9) mU/mL in CHC and 21.4 (17.4) in the CHB group (normal range 0.7-9; p=0.049) and mean HOMA-IR was 3.1 (2.6) in CHC versus 4.7 (4.1) in the CHB group (normal range 0.12-4.61; p=0.036). HOMA-IR was significantly associated with fibrosis stage in the CHC group (p=0.015), but not in the CHB group. CONCLUSION: Hyperinsulinemia occurs in chronic viral hepatitis B and hepatitis C; insulin resistance is associated with stage of fibrosis in hepatitis C.

Congenital hypothyroidism in Iran.

OBJECTIVE: Following elimination of iodine deficiency in Iran, the program of screening for congenital hypothyroidism (CH) was established in 1998. The descriptive findings of the study are reported here. METHODS: From February 1998 to June 2001, cord blood spot samples from 8 hospitals and a rural birth center in Tehran and Damavand were collected and tested for TSH measurement using a two-site IRMA method. TSH values > or = 20 microU/mL were recalled. The diagnosis of CH was confirmed using age adjusted reference values for serum TSH and T4 levels. RESULTS: Of 20107 screened neonates, 256 had cord TSH values > or = 20 microU/mL (recall rate: 1.3%) and 22 showed hypothyroidism (1:914 live births). History of maternal ingestion of drugs and dietary goitrogens were negative and minimal, respectively. 15 out of 21 CH neonates had parental consanguinity. The odds ratio of CH occurrence in blood-related to non-related marriages was 6.9 (CI=1.82-25.87). Thyroid dysgenesis occurred in 10 neonates; 1:2011 births. Urinary iodine excretion was between 12-22 (n=3) and 40-42.5 (n=5) microg/dL in 10 eutopic neonates (2 not assessed). CONCLUSION: Parental consanguinity and iodine excess could be the causative factors for the high incidence of CH.