Independent association of FTO rs9939609 polymorphism with overweight and obesity in Polish adults. Results from the representative population-based WOBASZ study.

Genetic factors play an important role in the origin of obesity. We investigated the association between the FTO rs9939609 genotype and overweight and obesity, along with additional anthropometric variables in the representative sample of adult Polish population. We genotyped a random sample of 3369 adult individuals examined in a cross-sectional population survey (WOBASZ 2003-2005). More than 40% of men and women had at least one A allele. The AA genotype was found in approximately one fifth of both men and women. The frequency of the AA genotype increased with higher BMI in both sexes and was associated with higher anthropometric obesity indicators in both men and women. The FTO rs9939609 AA genotype was significantly related to abnormal BMI [OR=1.55 (1.14-2.11)] and overweight [OR=1.55 (1.11-2.16)] or obesity [OR=1.56 (1.04-235)] in men regardless of age, tobacco smoking, physical activity, diet and diabetes, while in women it was related to abnormal BMI [OR=1.45 (1.05-2.01)] and overweight [OR=1.59 (1.11-2.29)] after adjustment in addition for menopause. The frequency of the A allele in the Polish population was the same as in other European countries. About one fifth of both men and women have the FTO rs9939609 AA variant. A significant relationship was found between the FTO genotype and anthropometric obesity indicators. The AA genotype was significantly associated with abnormal BMI and overweight in both sexes, but the relation to the obesity phenotype was observed only in men.

Prevalence of diabetes and impaired fasting glucose in Poland in 2005-2014: results of the WOBASZ surveys.

AIMS: To evaluate the prevalence of diabetes and impaired fasting glucose in Poland in 2013-2014 and to determine the temporal trends between 2003-2005 and 2013-2014. METHODS: A questionnaire survey was conducted in a representative sample of Polish adults, complemented by anthropometric and fasting plasma glucose measurements. The research was part of the national cross-sectional WOBASZ study. Diabetes was assessed as self-reported or screened (fasting plasma glucose level ≥ 7 mmol/l, based on one blood sample). RESULTS: In the years 2013-2014 among 5694 participants aged 20-74 years, 6.0% (95% CI 5.4-6.6) reported a previous diagnosis of diabetes (5.8% in women and 6.2% in men). In addition, 2.4% of the participants (95% CI 2.0-2.8) without a previous diagnosis of diabetes (1.8% of women and 3.1% of men) had a fasting blood glucose level ≥7.0 mmol/l in a single measurement. In a single measurement, 18.4% of the participants (95% CI 17.4-19.4; 13.2% of women and 23.8% of men) had impaired fasting glucose. The prevalence of dysglycaemia in the WOBASZ II study was significantly higher compared to the WOBASZ I study findings from 2003-2005, increased from 6.6% to 8.4% for diabetes and from 9.3% to 18.4% for impaired fasting glucose (after age and sex standardization to the 2013 Polish population). CONCLUSIONS: The prevalence of diabetes in Poland is similar to that observed in other European populations and has increased significantly over the last decade.

Properties and interaction of heterologously expressed glutamate decarboxylase isoenzymes GAD(65kDa) and GAD(67kDa) from human brain with ginkgotoxin and its 5'-phosphate.

Two isoforms of glutamate decarboxylase (GAD(65kDa) and GAD(67kDa)) from human brain, which had previously been overexpressed in Escherichia coli as fusion proteins containing a glutathione-S-transferase domain, were purified by affinity chromatography on glutathione Sepharose 4B. Both isoforms were also expressed in Saccharomyces cerevisiae. After modification of a HPLC based assay, the enzymes were characterized with respect to their biochemical properties. Comparison of kinetic data, pH, and temperature optima as well as of the mode of interaction with pyridoxal phosphate as a cofactor revealed several significant differences between the two isoenzymes reflecting their somewhat different physiological and molecular features. Investigation of the influence of 4'-O-methylpyridoxine (ginkgotoxin) (1), a neurotoxin occurring in Ginkgo biloba L., on the different isoenzymes, indicates that the phosphorylated form of the toxin, 4'-O-methylpyridoxine-5'-phosphate (2), decreases GAD(65kDa) activity, although in unphysiologically high concentrations, whereas GAD(67kDa) activity seems to be hardly affected.

Urinary kallikrein in rats bred for susceptibility and resistance to the hypertensive effect of salt and in New Zealand genetically hypertensive rats.

Urinary kallikrein excretion was studied in rats bred for susceptibility and resistance to the hypertensive effect of salt. The rats were on a regular rat chow diet (0.45% sodium content) and tap water and were not hypertensive at the time of the study. Urinary kallikrein excretion, measured by kinin radioimmunoassay, was 10 to 20 times lower in the susceptible rats than in the resistant rats (4.39 +/- 1.61 microgram/24 hours and 56.4 +/- 5.8 microgram/24 hours, respectively; P less than 0.001). Urinary kallikrein excretion was also measured in New Zealand genetically hypertensive rats and in normotensive Wistar-Otago rats (controls). Kallikrein was found to be significantly lower in the genetically hypertensive rats than in the controls (49.1 +/- 6.2 microgram/24 hours and 76.8 +/- 6.9 microgram/24 hours, respectively); however, when expressed per 100 g of body weight, there was no significant difference. In conclusion, although urinary kallikrein excretion per rat was decreased in the genetically hypertensive rats when compared with the controls, this difference could be caused by the lower body weight of the genetically hypertensive rats. Urinary kallikrein excretion, when expressed per 100 g of body weight, is significantly lower in susceptible than in resistant rats. This could be a consequence of a genetic defect that may play a role in the development of hypertension, perhaps through alteration of renal function.