Association of sweet taste receptor gene polymorphisms with dental caries experience in school children.

Sweet taste is a powerful factor influencing food acceptance. The peripheral taste response to sugar is mediated by the TAS1R2/TAS1R3 taste receptors. The aim of the study was to determine the relationship between TAS1R2 (rs35874116 or rs9701796) and/or TAS1R3 (rs307355) single nucleotide polymorphisms with dental caries experience in schoolchildren. A total of 184 schoolchildren aged between 7 and 12 years (101 girls, 83 boys) were included in the study. Genomic DNA was extracted from saliva samples and the genotypes were identified by qPCR. The genotype frequencies were as follows: 6.6% for homozygous wild type, 41.8% for heterozygous and 51.6% for homozygous polymorphic genotype carriers of TAS1R2 gene rs35874116; 27.8% for heterozygous and 72.2% for homozygous polymorphic genotype carriers of TAS1R2 gene rs9701796, and 83.1% for homozygous wild type and 16.9% for heterozygous genotype carriers of TAS1R3 gene rs307355 polymorphism. A significant association was observed between total caries experience (dft + DMFT - decayed filled primary teeth + decayed, missing and filled permanent teeth) and TAS1R2 rs35874116 (p = 0.008) and TAS1R3 rs307355 (p = 0.04) gene polymorphisms but not for TAS1R2 gene rs9701796 polymorphism. TAS1R3 gene rs307355 polymorphism has been found to be an independent risk factor for dental caries experience by logistic regression analysis and to have increased the risk of caries. Moderate caries experience (4-7 caries) was found to be associated with TAS1R3 rs307355 heterozygous genotype, whereas high-risk caries experience (>8 caries) was found to be associated with TAS1R2 rs35874116 homozygous polymorphic genotype.

Lipoprotein lipase gene PvuII polymorphism serum lipids and risk for coronary artery disease: meta-analysis.

Our aim was to determine whether lipoprotein lipase gene PvuII polymorphism can be considered as an independent risk factor for coronary artery disease (CAD) by conducting a meta-analysis of all available published trials, including our own study. In 7 seperate studies, 3289 subjects were screened for this substitution; meta-analysis included only some of these individuals. Among the 7 studies, 6 were performed on white subjects, whereas 1 was on patients with Saudi Arabic descent.Subgroup analysis indicated that individuals with PvuII substitution does not have an increased risk for CAD. The LPL-PvuII genotype and allele frequency distributions did not differ significantly between CAD patients and healthy controls. There was no difference in the distribution of LPL-PvuII genotypes between the healthy subjects and the patients with CAD. However, no significant differences in lipid variables (triglyceride and HDL-cholesterol) were determined for the PvuII polymorphisms in the patients with CAD. No significant differences were found in serum triglyceride and HDL-cholesterol levels for LPL-PvuII genotypes when the control and CAD groups were pooled. In conclusion, LPL-Pvu II polymorphism cannot be used as independent genetic risk factor for CAD.

Protective effects of a calcium channel blocker on apoptosis in thymus of neonatal STZ-diabetic rats.

Streptozotocin (STZ) is known to induce insulin-dependent diabetes in experimental animals. In STZ-induced diabetes, atrophy of the thymus is caused by elevated intracellular calcium levels leading to apoptosis. Hyperglycemia is known to result in a decrease in numbers of T cells in the thymus and circulation. Intracellular calcium levels increase in diabetic animals after induction by STZ. Hyperglycemia inhibits Ca2+-ATPase and increases intracellular calcium levels. We have investigated apoptosis in thymus tissue of neonatal STZ (n-STZ)-diabetic rats and the effects of isradipine as a calcium channel blocker (CCB) on apoptosis. Five groups of newborn Wistar rats were used. On the second day after birth, 100 mg/kg STZ was given i.p. to the first two groups. The first group was n-STZ diabetic. To the second group, starting from the 12th week, 5 mg/kg/day isradipine (i.p) was given for 6 weeks. To the third group, the same dose of isradipine was given on the second day, followed by STZ treatment. The fourth group was non-diabetic and treated with 5 mg/kg/day isradipine for six weeks. The fifth group consisted of non-diabetic rats. To the sixth group, dexamethasone (5 mg/kg i.p.) was given to adult rats. For detection of apoptotic cells in paraffin-embedded thymus sections, the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) assay was used. The DNA ladder method was performed for analysis of DNA fragmentation. In the isradipine-treated non-diabetic group, typical apoptotic banding patterns were found, whereas thick bands between 123 and 246 bp length were found in the n-STZ- and n-STZ+isradipine-treated groups. More apoptotic cells were observed in the thymus of isradipine-treated, n-STZ-treated and n-STZ+isradipine-treated groups when compared with the non-diabetic control and isradipine+n-STZ-treated groups. In conclusion, we observed that long-term STZ diabetes results in apoptosis in the thymus. We also found that isradipine administered before STZ has protective effects against apoptosis, whereas isradipine alone induces apoptosis.

The relationship of Bradykinin B2 receptor gene variation with obesity, hypertension and lipid variables in obese patients.

OBJECTIVE: This study examined the association of C-58T genotypes with obesity/hypertension related parameters and serum lipids in obese (n=108) and non-obese (n=80) patients. MATERIALS AND METHODS: Bradykinin receptor (B2R) C-58T genotypes were determined by PCR-RFLP. RESULTS: B2R gene C-58T frequencies for T/T (homozygous wild type), T/C (heterozygous) and C/C (homozygous polymorphic) genotypes for obese and non-obese patients were respectively: 36.1%, 37.5%; 45.4%, 52.5% and 18.5%, 10%. Obese patients using diuretic medication had lower C/C genotype frequency compared to T/T and T/C genotypes. Total cholesterol (T-Chol) (p=0.035) levels were found to be associated with B2R C-58T polymorphism, where the T/T genotype had higher total cholesterol levels compared to the T/C genotype in obese patients. Non-obese patients using oral antidiabetic medication had higher C/C genotype frequency than that of T/T and T/C genotypes. Waist circumference (p=0.016) and diastolic blood pressure (p=0.01) levels were elevated in the non-obese subjects with the C/C genotype compared to T/C and T/T. CONCLUSION: Although B2R C-58T gene polymorphism was not found to be effective on obesity with logistic regression analysis in the whole study population in obese subjects, the T-Chol decreasing effect of the B2R gene C allele and the higher waist circumference measurements in the non-obese subjects may indicate there may be a link between B2R gene C-58T polymorphism and obesity in study populations of higher numbers.

Prevalence of endothelial nitric oxide synthase E298D polymorphism in Turkish patients with essential hypertension.

AIMS: Our aim was to evaluate the effects of endothelial nitric oxide synthase (eNOS) E298D polymorphism in obesity variables and essential hypertension (eHT) development risk. The genotype frequencies of E298D polymorphism in eHT patients and non-hypertensive (non-HT) controls (proven to have normal coronaries angiographically) were analyzed for their association with demographic and obesity related data of the eHT patients and controls. MATERIALS AND METHODS: eNOS gene E298D genotypes were determined with qPCR. RESULTS: The eNOS E298D polymorphism frequencies for 298E/E, 298E/D and 298D/D genotypes were respectively as 41.1%, 44.6%, 14.3% in subjects eHT and 52.8%, 38.9%, 8.3% in the non-HT groups. The combined E298D homozygous polymorphic and heterozygous genotypes were found to have a decreasing effect on serum total-cholesterol levels in comparison to wild-type genotypes in eHT patients but not controls. CONCLUSIONS: Our results support the idea that, the eNOS E298D polymorphism, which is not associated with hypertension, may increase the risk of hypertension when associated with high serum total-cholesterol levels.

Relationship of RIC-3 gene rs1528133 polymorphism with varying degrees of body weight and eating behavior.

AIMS: The aim of this study was to determine the allele frequencies of resistance to inhibitors of cholinesterase 3 homologue (RIC-3) gene rs1528133 polymorphism in overweight+obese+morbid obese and non-obese (non-OB) subjects. The effects of rs1528133 genotypes on anthropometric, diabetes and obesity related parameters, self-reported macronutrient intake and drugs were also evaluated. The study was performed on overweight+obese+morbid obese and non-obese subjects. METHODS: RIC-3 gene rs1528133 genotypes were determined with qPCR. RESULTS: The RIC-3 rs1528133 genotype frequencies were respectively as 89.4% for homozygous wild type (A/A), 10.6% for heterozygous (A/C) genotypes in overweight+obese+morbid obese patients and 92.7% for A/A, 7.3% for A/C genotypes in non-OB subjects. The homozygous mutant genotype (C/C) was not detected in our study population. Genotype frequencies were not significantly different among study groups. Heterozygous genotype carriers for the rs1528133 polymorphism were found to prefer higher glycemic load, fat and protein diet content compared to homozygous wild type genotype carriers (p=0.0001). The frequency of rs1528133 heterozygous individuals (16.7%) using antihypertensive drugs was lower (p=0.045) in comparison to wild type genotype carriers (46.9%) in the whole study population. CONCLUSIONS: RIC-3 gene rs1528133 variation was not found to be effective over any analyzed obesity related parameter, but associated with higher glycemic load, protein and fat eating behavior and antihypertensive drug use.

FTO mRNA expression in extremely obese and type 2 diabetic human omental and subcutaneous adipose tissues.

BACKGROUND: Fat mass and obesity-associated protein (FTO) gene expression is known to correlate with obesity. Our aim was to investigate the FTO gene expression in paired omental and subcutaneous human adipose tissues from morbid and obese patients. To understand the role of CD68-positive macrophages in adipose tissues, the correlation with adiposity parameters such as adipocyte diameter and adipocyte radius was also measured. Drug and adiposity correlations were also analyzed. METHODS: Paired omental and subcutaneous adipose tissue were excised during elective surgery from morbidly obese (n = 9) and obese (n = 5) patients. FTO expressions were determined by quantitative PCR. Tissue sections were analyzed for their CD68 protein expressions by immunuhistochemistry. RESULTS: Omental and subcutaneous adipose tissue FTO gene expression levels were not found to differ significantly among morbidly obese and obese study groups. Serum aspartate aminotransferase e and alanine transaminase levels were found to be in negative correlation with subcutaneous fat tissue FTO expression rate. Antidiabetic drug use was found to be in correlation with adiposity. Both subcutaneous and omental fat cell diameters were found to have correlation with antidiabetic drug use. Omental fat cell diameter was found to enlarge together with omental CD68 protein expression. Subcutaneous macrophage number decreased while omental fat cell radius increased. Omental macrophage number was found in correlation with subcutaneous macrophage number. CONCLUSIONS: Antidiabetic therapy was found to increase adiposity in omental and subcutaneous fat. Further research is needed with larger samples to explore the exact role of FTO in obesity.

Presence of fatty-acid-binding protein 4 expression in human epicardial adipose tissue in metabolic syndrome.

BACKGROUND: Metabolic syndrome is a cluster of different clinical manifestations that are risk factors for atherothrombotic cardiovascular disorders. Fatty-acid-binding protein 4 (FABP4/aP2), which is highly expressed in adipocytes, specifically exerts intracellular lipid trafficking. A high level of fatty-acid-binding protein 4 expression present in obese subjects has also been found in mice and humans, especially in macrophages at atherosclerotic lesions. An in vivo study demonstrated that the inhibitor of aP2 would be a new therapeutic agent for treating metabolic diseases in mice. We have investigated the mRNA expression of fatty-acid-binding protein 4 in human epicardial adipose and ascending aorta tissues of metabolic syndrome and nonmetabolic syndrome patients. METHODS: Paired epicardial adipose and ascending aorta tissue samples were obtained from 10 metabolic syndrome patients and 4 nonmetabolic syndrome patients during coronary bypass grafting and aortic valve replacement therapy, respectively. Fatty-acid-binding protein 4 gene expression was determined by quantitative real-time polymerase chain reaction. RESULTS AND CONCLUSIONS: Fatty-acid-binding protein 4 expression of epicardial adipose tissue was significantly higher in metabolic syndrome patients than in nonmetabolic syndrome controls (P<.05). In metabolic syndrome patients, fatty-acid-binding protein 4 expression in epicardial adipose tissue was 66 times higher than fatty-acid-binding protein 4 expression in ascending aorta tissue. The expression level of fatty-acid-binding protein 4 in epicardial adipose tissue was found to be significantly correlated with waist circumference in all subjects (r=.535, P<.05). Our data showed for the first time that human epicardial adipose and ascending aorta tissues express fatty-acid-binding protein 4 and that its level of expression in epicardial adipose tissues of metabolic syndrome patients is elevated. Increased fatty-acid-binding protein 4 gene expression in epicardial adipose tissues of metabolic syndrome patients led us think that fatty-acid-binding protein 4 might be an important factor in metabolic syndrome.

DNA polymorphism of Pvu II site in the lipoprotein lipase gene in patients with non-insulin dependent diabetes mellitus.

We studied the effect of variation at the lipoprotein lipase (LPL) gene locus on the susceptibility of individuals with non-insulin dependent diabetes mellitus (NIDDM) in a population of 110 NIDDM patients and 91 controls. Our objective was to study the relationship between the LPL-Pvu II polymorphism and NIDDM and lipid metabolism. PCR-RFLP was used to determine the DNA polymorphism of the sixth intron of the LPL gene. The frequencies of the genotypes in case and control groups were 29.1 and 30.8% for P+/P+; 45.5 and 36.3% for P+/P-; 25.5 and 33% for P-/P- respectively. There was no significant difference in frequencies of genotypes between the two groups. Logistic regression analysis revealed that triacylglycerol (TAG) and apolipoprotein E levels were associated with NIDDM, whereas Pvu II genotypes were not found as independent risk factors for the disease. Overall this study demonstrates the role of the Pvu II polymorphism in the LPL gene in modulating plasma lipid/lipoprotein levels in patients with NIDDM.