Effect of MDR C3435T polymorphism on Varenicline treatment in quit smoking

Despite so many global efforts, smoking still remains to be one of the most common addictions worldwide. Even though most smokers wish to quit smoking, many of them fail. In this respect, genetic variants are thought to be remarkable factors in nicotine dependence and in treatment of smoking cessation. This is a paper investigating a single variant p-glycoprotein (P-gp) polymorphisms and its effect on Varenicline efficacy in the smoking cessation. 158 smokers and 52 non-smoker healthy volunteers were included. We determined the P-gp C3435T gene polymorphisms in all subjects. Face to face interviews with smokers were performed for smoking cessation and Varenicline was given for smoking cessation. Cessation success was evaluated in the 6th month and success rates were compared according to the P-gp genotype distributions. In our study, smoking cessation rate by Varenicline was 57.0%. This rate was 55.0% in females, and 57.2% in males (p=0.85). The P-gp C3435T gene distribution was similar in control, quitters and not-quitter groups. Cessation rate was at highest point in genotype CT (62.2%) and at the lowest in TT (47.6%). It was 53.8% in genotype CC and there was no statistically significant difference (p=0.27). Our results suggest that genetic variants of P-gp C3435T did not significantly affect Varenicline treatment for smoking cessation.

Effect of acute and chronic exercise on plasma matrix metalloproteinase and total antioxidant levels.

The relationship between acute and chronic exercise and expression of matrix metalloproteinases (MMPs) in muscles is unknown. There happen some alterations in the oxidant-antioxidant balance due to exercise. This study aimed to investigate the levels of MMP-1, tissue inhibitors of metalloproteinases (TIMP-1), hyaluronic acid (HA), total antioxidant status (TAS), and total oxidant status (TOS) following acute and chronic exercising in rats. Twenty-six Wistar Albino male rats were divided in to three groups: control, acute, and chronic groups. In acute group, treadmill exercise was performed 3 days/wk, 10 min/day for 1 week. In chronic group, exercise performed 7 days/wk, 60 min/day for 4 weeks. At the end of the experiment, plasma MMP-1, TIMP-1, HA, TAS, and TOS levels were measured. In current study, the MMP-1, TIMP-1, HA, and TOS levels not observed statistically significant difference among all groups, but in chronic group, there was a significantly difference (P<0.05) between the control and experimental groups in terms of TAS and oxidative stress index (OSI) levels. TAS, TOS, and OSI levels were significantly different between control and chronic exercise group (P<0.01, P<0.05, and P<0.01, respectively). According to these results, we can say acute and chronic exercise does not effect on plasma MMP-1, TIMP-1, and HA levels.

Examination of levels pentraxin-3, interleukin-6, and C-reactive protein in rat model acute and chronic exercise.

Different types of exercise occurs damage at the cellular level in the muscles. Muscle damage caused by exercise is determined creatine kinase, myoglobin, and increase in levels of acute phase protein and interleukin in blood. The purpose of this study was investigated the levels of pentraxin-3 (PTX-3), interleukin-6 (IL-6), and C-reactive protein (CRP) following acute and chronic exercising in rats. Twenty-six Wistar Albino male rats were divided in to three groups. A treadmill exercise was performed 3 days/week, 10 min/day for 1 week in acute groups. In chronic group, exercise performed 7 days/week, 60 min/day for 4 weeks. At the end of the experiment, plasma PTX-3, IL-6, and CRP levels were measured. In current study, the PTX-3, IL-6, and CRP levels not observed statistically significant difference among control, acute, and chronic groups. The levels IL-6 and CRP were not significantly different between acute and chronic exercise groups (P>0.05). However, the level of PTX-3 was found to be higher in the chronic group compared to the acute group (P<0.05). The PTX-3 level increase on chronic exercise-induced muscle damage. Accorting to our results, we think that PTX-3 may have a protect role on muscle damage during chronic exercises.

Leptin Receptor Gene Polymorphism may Affect Subclinical Atherosclerosis in Patients with Acromegaly.

BACKGROUND: Acromegaly is associated with increased morbidity and mortality related to cardiovascular diseases. Leptin (LEP) and Leptin Receptor (LEPR) gene polymorphisms can increase cardiovascular risks. The aim of this study was to investigate association between the frequencies of LEP and LEPR gene polymorphisms and subclinical atherosclerosis in acromegalic patients. METHODS: Forty-four acromegalic patients and 30 controls were admitted to study. The polymorphisms were identified by using polymerase chain reaction from peripheral blood samples. The levels of systolic and diastolic blood pressure, BMI, fasting plasma glucose, fasting insulin, IGF-I, GH, IGFBP3, leptin, triglyceride, carotid Intima Media Thickness (cIMT) and HDL and LDL cholesterol concentrations were evaluated. RESULTS: There was statistically significant difference between the LEPR genotypes of acromegalic patients (GG 11.4%, GA 52.3%, and AA 36.4%) and controls (GG 33.3%, GA 50%, and AA 16.7%) although their LEP genotype distribution was similar. In addition, the prevalence of the LEPR gene G and A alleles was significantly different between patients and controls. No significant difference was found among the G(-2548) A leptin genotypes of groups in terms of the clinical parameters. cIMT significantly increased homozygote LEPR GG genotype group compared to AA subjects in patients. But the other parameters were not different between LEPR genotypes groups of patients and controls. CONCLUSION: It can be said that the LEPR gene polymorphism may affect cIMT in patients. The reason is that LEPR GG genotype carriers may have more risk than other genotypes in the development of subclinical atherosclerosis in acromegaly.

Effect of Erythropoietin and Stem Cells on Traumatic Brain Injury.

OBJECTIVE: To investigate the healing effects of erythropoietin (EPO) and stem cells (SCs) in traumatic brain injury (TBI). METHODS: Twenty-nine Wistar albino rats were used and separated into the following groups: control (C), EPO, SC, and SC+EPO. Group C received a TBI only, with no treatment. In the EPO group, 1000 U/kg EPO was given intraperitoneally at 30 minutes after TBI. In SC group, immediately after formation of TBI, 3 × 10,000 CD34(+) stem cells were injected into the affected area. In the SC+EPO group, half an hour after TBI and the injection of stem cells, 1000 U/kg EPO was injected. Before and after injury, trauma coordination performance was measured by the rotarod and inclined plane tests. RESULTS: Seven weeks after trauma, rat brains were examined by radiology and histology. Rotarod performance test did not change remarkably, even after the injury. Compared with group C, the SC+EPO group was found to have significant differences in the inclined plane test results. CONCLUSIONS: Separately given, SCs and EPO have a positive effect on TBI, and our findings suggest that their coadministration is even more powerful.

Angiotensinogen gene M235T and angiotensin II-type 1 receptor gene A/C1166 polymorphisms in chronic obtructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) occurs irreversibly and is characterized by progressive airflow obstruction. Renin angiotensin system (RAS) has many different key enzymes and receptors that have a role for different systemic processes. We aimed to determine genotype and allele frequencies of angiotensinogen (AGT) M235T and angiotensin II-type 1 receptor (AT1-R) A/C1166 polymorphisms in patients with COPD. This study was performed on 56 unrelated COPD patients and 29 healthy subjects. DNA samples for each individual were isolated from peripheral blood by phenol/chloroform method, analyzed by polymerase chain reaction and enzymatic digestion methodologies. The distribution for each of AGT genotypes were 23.2% for MM (13), 75.0% for MT (42) and 1.8% for TT (1) in the COPD group; 37.9% for MM (11), 34.5% for MT (10) and 27.6% for TT (8) in the control group. The distribution of AGT genotypes was found significantly different between groups (X(2) = 18.604; df = 2; P = 0.000). The frequencies for each of the AT1-R genotypes were found as 53.6% for AA (30), 42.9% for AC (24), 3.6% for CC (2) in the COPD group; 55.2% for AA (16), 41.4% for AC (12) and 3.4% for CC (1) in the control group. The distribution of AT1-R genotypes did not change significantly between groups. Allele frequencies of interested genes were not significantly different between groups. We suggest that AGT polymorphism may play a role for the development of COPD. We believe these data can be served for large scale population genetics research, considering the frequency of AGT and AT1-R genes and alleles in COPD patients in the Turkish population.

The effect of chronic peripheral nesfatin-1 application on blood pressure in normal and chronic restraint stressed rats: related with circulating level of blood pressure regulators.

Nesfatin is a peptide secreted by peripheral tissues, central and peripheral nervous system. It is involved in the regulation of homeostasis. Although the effects of nesfatin-1 on nutrition have been studied widely in the literature, the mechanisms of nesfatin-1 action and also relations with other physiological parameters are still not clarified well. We aimed to investigate the effect of peripheral chronic nesfatin-1 application on blood pressure regulation in normal and in rats exposed to restraint immobilization stress. In our study, three month-old male Wistar rats were used. Rats were divided into 4 groups as Control, Stress, Control+Nesfatin-1, Nesfatin-1+Stress. Angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone, cortisol, nesfatin-1 levels were determined in plasma samples by ELISA. Our results have shown that chronic peripheral nesfatin-1 administration increases blood pressure in normal and in rats exposed to chronic restraint stress. Effect of nesfatin-1 on circulating level of angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone and cortisol has been identified. We can conclude that elevated high blood pressure after chronic peripheral nesfatin-1 administration in rats exposed to chronic restraint stress may be related to decreased plasma level of endothelial nitric oxide synthase concentration.

MDR-1 gene C/T polymorphism in COPD: data from Aegean part of Turkey.

OBJECTIVE: Genetic factors, in addition to oxidative stress factors, have been implicated in the development of chronic obstructive pulmonary disease (COPD). Multi-drug resistant-1 (MDR-1) is a gene located on chromosome 7 and the products of this gene protect lung tissue from oxidative stress. We searched the frequency of MDR-1 gene C/T polymorphism in patients with COPD and aimed to explain the association between MDR-1 gene and COPD development. METHODS: 47 patients with COPD and 64 healthy control participants were placed in this study. DNAs were extracted from blood samples and MDR-1 amplification of DNA was performed using polymerase chain reaction and enzyme digestion techniques. RESULTS: The frequencies of MDR-1 genotypes were found 17.0% for CC, 51.1% for CT and 31.9% for TT in the COPD group and 39.1% for CC, 53.1% for CT and 7.8% for TT in the control group. The distribution of MDR-1 gene C alleles were found 32.3% in COPD group and 67.7% in control group; T alleles were found 55.1% in COPD group and 44.9% in control group. There was statistically significant difference between the groups for genotype and allele frequency of MDR-1 gene (P = 0.001). CONCLUSION: TT genotype of MDR-1 gene was significantly more frequent in COPD patients. MDR-1 gene C/T polymorphism may play a role in COPD development.

Orexins cause epileptic activity.

Orexins have been implicated in the regulation of sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on epileptic activity are controversial. We investigated whether intracortical injections of orexin A (100 pmol) and B (100 pmol) cause epileptic activity in rats. We observed epileptic seizure findings on these two groups rats. Orexin A and B also significantly increased total EEG power spectrum. Our findings indicate that orexins cause epileptic activity.

Orexins increase penicillin-induced epileptic activity.

Orexins have been implicated with physiological function including sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on excitability are controversial. We investigated the effects of intracortical injections of orexin A (100 pmol) and B (100 pmol) on the electrophysiological manifestation of epileptic seizures induced by cortical penicillin application in adult male rats. In comparison to saline, orexin A and B enhanced significantly the spike number, spike amplitude and spectral power values induced by cortical penicillin. Our findings indicates that orexins enhances the hyperexcitable and hypersyncronic cortical epileptic activity induced by focal application of penicillin-G.

Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks.

BACKGROUND: Aluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain. MATERIAL/METHODS: We used a chick embryonic development model, with Al treatment of 500 µg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool. RESULTS: This Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model. CONCLUSIONS: Exposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

The growth hormone receptor polymorphism in patients with acromegaly: relationship to BMI and glucose metabolism.

The aim of this study was to investigate association between the frequencies of Growth Hormone receptor (d3GHR) gene polymorphisms and some clinical parameters of acromegalic patients. Total of 35 acromegalic patients were enrolled to study. The d3GHR polymorphism was identified by using polymerase chain reaction from peripheral blood samples. The levels of systolic and diastolic blood pressure, BMI, fasting plasma glucose (FPG), Fasting insulin, HOMA-IR, IGF-I, GH, IGFBP3, triglyceride, HDL and LDL cholesterol concentrations were evaluated. The frequencies of d3GHR genotypes were found as follows; 5 (14.3%) subjects had d3/d3, 11 (31.4%) had d3/fl and 19 (54.3%) had fl/fl in patients. The prevalence of the d3 and fl alleles was 30 and 70%, respectively. Systolic blood pressure, fasting insulin and HOMA-IR was found significantly increased in homozygote d3GHR genotype group compared to d3/fl subjects (P < 0.05). In addition, BMI was observed significantly different among three genotypes (P = 0.007) and in the subjects with d3/d3 genotype, BMI was found significantly higher than d3/fl and fl/fl genotypes groups. As well as, no significant difference was found between the d3 and fl alleles group in terms of the clinical parameters except for BMI (P = 0.002). It can be said that the d3GHR gene polymorphism may affect BMI, systolic blood pressure and insulin regulation. At the same time we can say homozygote d3GHR genotype and d3 allele carriers may have more risk than other genotypes for high BMI.

Angiotensin converting enzyme I/D, angiotensinogen M235T and AT1-R A/C1166 gene polymorphisms in patients with acromegaly.

Acromegaly is associated with increased morbidity and mortality related to cardiovascular disease. Hypertension is one of the most common cardiovascular risk factors in acromegalic patients. The aim of this study was to investigate association between the frequencies of angiotensin converting enzyme (ACE) I/D, angiotensinogen (AGT) M235T and the angiotensin II type 1 receptor (AT1-R) A/C1166 gene polymorphisms and some clinical parameters of acromegalic patients. Total of 33 acromegalic patients and 63 controls were enrolled to study. We determined the ACE I/D, AGT M235T and AT1-R A/C1166 gene polymorphisms. Serum insulin, glucose, triglyceride, HDL-cholesterol, LDL-cholesterol, growth hormone and Insulin-like growth factor I (IGF-I) levels of subjects were analyzed. The frequencies of ACE and M235T AGT genotype were not significantly different between control and patients. The distribution of AT1R A/C1166 genotypes was significantly different between patients and control subjects (P=0.016). None of the three ACE genotypes, DD, ID and II displayed significant difference in acromegalic patients. A significant difference in systolic blood pressure and the serum IGF-I levels among the three AGT genotype, MM, MT and TT genotypes was found in patient group. Individuals with MT genotypes had significantly higher serum IGF-I levels and systolic blood pressure than MM and TT genotype subjects, P<0.05. In addition, serum triglyceride and HDL levels differed significantly between MM and MT genotypes, P<0.05. However, systolic blood pressure of patients with CC genotypes was found to be significantly higher than AA genotypes individuals in acromegaly group, P<0.05. It can be said that the angiotensinogen MT and AT1R CC1166 genotype carriers may have more risk than other genotypes in the development of hypertension in acromegaly.

The effects of docosahexaenoic acid supplementation and exercise on growth hormone and insulin-like growth factor I serum levels during chronic hypoxia in rats.

BACKGROUND: In this study we examined the effects of docosahexaenoic acid (DHA) on growth hormone (GH), insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) in response to chronic hypoxia and exercise training in hypoxic conditions. METHODS: Thirty-five rats were divided into five groups; control group (C), hypoxia group (H), hypoxia-exercise group (HE), hypoxia-docosahexaenoic acid group (HD), hypoxia-exercise-docosahexaenoic acid group (HED). A treadmill exercise was performed as 30 m/min for 20 min/day, 5 days per week for 28 days at level grade for the exercising groups (HE and HED). DHA was given to the HD and HED groups every day orally (36 mg/kg). The animals, except for the C group, were exposed to hypoxia for 28 days. RESULTS: Serum levels of GH and IGF-I in the H group decreased after chronic hypoxia (p<0.001). GH and IGF-I in the HD group also decreased compared with the C group (p<0.05, p<0.01, respectively). GH in C group did not show significant difference compared with the HE and HED groups. Decreased serum level of IGF-I was observed for the HED group (p<0.05). CONCLUSIONS: According to our findings, chronic hypoxia exposure decreases serum levels of GH, and IGF-I and exercise training have a slightly positive effect on GH/IGF-I axis during hypoxia. In addition, DHA supplementation slightly increases GH and IGF-I serum levels in hypoxic conditions. However, this effect on GH/IGF-I axis during hypoxia is not strong compared with exercise. Therefore, we concluded that exercise and/or DHA supplementation does not have additional positive effect on these hormones in hypoxic conditions.

Cadmium intoxication of pregnant rats and fetuses: interactions of copper supplementation.

BACKGROUND AND AIMS: Cadmium (Cd) is an industrial and environmental pollutant that was shown to be involved in the development of some diseases. Due to high amounts of Cd in cigarettes, smokers and passive smokers are exposed to high amount of Cd. We aimed to determine whether Copper (Cu) supplementation would have a protective effect against Cd intoxication in pregnant rats and their fetuses. METHODS: Experiments were performed on 27 adult female Wistar albino rats divided into three experimental groups. CdCl(2), CdCl(2) plus CuSO(4) and only drinking water was given to different groups for 21 days. We measured cadmium (Cd), malondialdehyde (MDA), reduced glutathione (GSH), myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) levels in dams' liver, dams' kidney, fetus liver, fetus kidney, and placenta of rats. RESULTS: In all tissues of Cd and Cd + Cu-treated groups, Cd levels were found to be increased significantly when compared to control group. MDA levels and MPO activities were significantly increased whereas GSH levels, activities of SOD and CAT were decreased in Cd groups when compared to control group. Cu supplementation significantly prevented the increment in MDA levels and brought MPO activities back to control levels or below. Cd-induced reductions in GSH levels and SOD activities were also prevented by Cu supplementation. An increase of CAT activity after Cu supplementation was enough to revert to the control levels in some tissues. CONCLUSIONS: Our findings suggest that Cu supplementation may have a protective effect against the Cd-induced oxidative stress in liver, kidney and placental tissues of pregnant rats and fetuses.

Angiotensin converting enzyme gene insertion/deletion polymorphism in patients with polycystic ovary syndrome.

OBJECTIVE: The aim of this study is to investigate the relevance of polymorphism in angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism to the pathophysiology of polycystic ovary syndrome (PCOS). SUBJECTS AND METHODS: Thirty patients with PCOS by Rotterdam consensus criteria and 33 control subjects were prospectively investigated. ACE gene amplification of DNA was performed by polymerase chain reaction. Homeostatic model assessment (HOMA-IR) was applied. RESULTS: Compared to controls, ACE gene DD genotype and D allele were observed more frequently in PCOS (63% vs. 46% for DD genotype and 75% vs. 67% for D allele) (p > 0.05). Body mass index, fasting glucose and insulin levels, HOMA-IR index and total testosterone levels were higher in PCOS group (p < 0.05). The frequencies of D and I alleles were 45 (75%) and 15 (25%) for PCOS group and 44 (67%) and 22 (33%) for control group (p > 0.05). No significant differences were observed in the genotype and allele distributions between cases and control groups. HOMA-IR index was significantly higher in patients with PCOS with DD genotype than those with II genotype (p < 0.05). CONCLUSION: The ACE gene polymorphism was not associated with PCOS. However, the presence of D allele was associated with higher rate of insulin resistance in patients with PCOS.

Angiotensin-converting enzyme gene polymorphism in overweight and obese Turkish patients with insulin resistance.

The aim of this study was to analyze the distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene in obese Turkish patients with insulin resistance (IR). Sixty-two obese Turkish patients with IR were enrolled in this study. One hundred healthy people without IR were recruited as the control group. ACE amplification was performed by polymerase chain reaction. The frequency of the DD genotype was significantly higher in obese patients with IR than in control subjects. Of sixty-two patients, 1 (1.6%) had an II genotype, 22 (35.5%) had an ID genotype, and 39 (62.9%) had a DD genotype. The frequency of the I allele in the patient group was significantly lower than in controls. We found that the frequency of the DD genotype was higher in obese Turkish patients with IR. ACE gene I/D polymorphism may be associated with obesity in the Turkish population.

The effects of copper sulfate on liver histology and biochemical parameters of term Ross broiler chicks.

Copper is an essential trace element that is extremely toxic to organisms and organs at high doses. We have investigated the histological and biochemical effects of a toxic dose of copper sulfate on the liver of term Ross broiler chicks. Fertilized eggs were divided into three groups: experimental, injected with 50 mcg/0.1 ml copper sulfate in the air chambers on day 1; sham, injected with 0.1 ml saline; and control, no injection. Term chicks were killed and their livers investigated histologically, with hematoxylin-eosin-stained sections examined under light microscopy, and biochemically, for malondialdehyde and glutathione levels. Histological examinations showed copper-treated samples with granular degeneration and necrosis of hepatocytes and impairment to the cell lining of the remark cords. The samples had a congestive appearance, with blood in the vena centralis and sinusoids, slight connective tissue increase, and lymphocyte infiltration. Control and sham group sections had normal appearances. As oxidative damage parameters, in the copper-treated group, malondialdehyde levels were increased and glutathione levels decreased. In the sham and control groups, there were no significant differences. At this toxic dose, copper sulfate shows oxidative damage according to the histology of term chick liver that are confirmed biochemically by the changes in malondialdehyde and glutathione levels.

Insulin-like growth factor-I gene and insulin-like growth factor binding protein-3 polymorphism in patients with thyroid dysfunction.

BACKGROUND AND AIMS: Thyroid hormones have important roles in normal growth and skeletal muscle development. IGF-I is one of the most important growth factors and is needed for the proliferation and development of thyroid cells. It stimulates fibroblasts, follicular and endothelia cells in thyroid gland. It has been shown that thyroid hormones play an important role in the regulation of IGF-I and IGFBP-3. In this study we proposed that IGF-I (CA)(19) and IGFBP-3-202 A/C gene polymorphism may affect thyroid functions. For this purpose, frequency of IGF-I (CA)(19) and IGFBP-3-202 A/C gene polymorphism in hypo- and hyperthyroid patients and possible role of these polymorphism in thyroid functions were investigated. METHODS: This study was performed on 37 volunteer hyperthyroid and 76 hypothyroid patients as well as with 50 healthy subjects as controls. DNA isolation was applied in peripheral blood samples obtained from patients and controls. Required areas were amplified with PCR by using proper primers belonging to these gene areas from the isolated DNA samples. The products were evaluated with visualization by UV gel documentation system. RESULTS: Frequency of IGF-I (CA)(19) gene polymorphism among hypothyroidism patients, hyperthyroidism patients and controls were statistically significant (chi(2) = 11.55, df = 4, p = 0.021). Genotypic variations between hyper- and hypothyroid patients were significant (chi(2) = 11.39, df = 2, p = 0.003), whereas there was no difference in IGF-I (CA)(19) gene polymorphism between the patients and controls. Differences in the IGFBP-3-202 A/C gene polymorphism between controls and hypo- as well as hyperthyroid patients were not significant. But IGFBP-3-202 A/C gene polymorphism genotype frequencies showed a significant difference between hypo- and hyperthyroid patients (chi(2) = 6.24, df = 2, p = 0.044). CONCLUSIONS: These findings suggests that IGF-I (CA)(19) and IGFBP-3-202 A/C gene polymorphisms may be a risk factor for hypothyroidism.

ACE gene polymorphism and cardiac structure in patients with insulin resistance.

AIMS: Angiotensin-converting enzyme (ACE) is a key enzyme in the production of angiotensin II, thus may participate in the modulation of cardiac growth. The aim of our study is to analyze the ACE gene I/D polymorphisms in patients with insulin resistance (IR) and to evaluate its relationship to left ventricular mass and functions. METHODS: Eighteen subjects (13 female and 5 male, mean age 39.8 +/- 14) with IR were enrolled in the present study. Twenty-three healthy people without IR were recruited as the control group. ACE amplification of DNA was performed by polymerase chain reaction methodology. Fasting glucose and insulin, postprandial glucose, homeostasis model assessment (HOMA-IR) and HOMA-beta, lipid profile, anthropometric measurements were assessed. Left ventricular structure and functions were measured by echocardiography. RESULTS: Distribution of I/D polymorphism of the ACE gene in the study group was as follows: genotype II-0%, ID-38.9%, DD-61.1% of patients. Distribution of individual genotypes was similar in patients with and without IR. No significant difference was found between genotype groups in terms of anthropometric measurements and metabolic parameters and blood pressure. Echocardiography showed no significant changes in left ventricular structure and functions in patients with IR. CONCLUSIONS: We considered that in patients with IR, there is no relationship between I/D polymorphism of the ACE gene and LVH.