MTNR1B Genetic Variability Is Associated with Gestational Diabetes in Czech Women.

The gene MTNR1B encodes a receptor for melatonin. Melatonin receptors are expressed in human ß-cells, which implies that genetic variants might affect glucose tolerance. Meta-analysis confirmed that the rs10830963 shows the most robust association. The aim of the study was to assess the rs10830963 in Czech GDM patients and controls and to study relations between the SNP and biochemical as well as anthropometric characteristics. Our cohort consisted of 880 women; 458 were diagnosed with GDM, and 422 were normoglycemic controls without history of GDM. Despite similar BMI, the GDM group showed higher WHR, waist circumference, abdominal circumference, and total body fat content. The risk allele G was more frequent in the GDM group (38.3 versus 29.4% in controls, OR 1.49 CI95% [1.22; 1.82]; P OR = 0.0001). In spite of higher frequency, the G allele in the GDM group was not associated with any markers of glucose metabolism. In contrast, controls showed significant association of the allele G with FPG and with postchallenge glycemia during the oGTT. Frequency analysis indicates that rs10830963 is involved in gestational diabetes in Czech women. However, the association of the SNP with glucose metabolism, which is obvious in controls, is covert in women who have experienced GDM.

Cigarette smoking and progesterone and androgen metabolites in premenopausal women.

BACKGROUND: Smoking represents the most widespread substance dependence in the world. Several studies show nicotine's ability to alter women hormonal homeostasis. Women smokers have higher testosterone and lower estradiol levels throughout life compared to women non-smokers. This negatively affects women's reproductive function. Furthermore, alteration of neuroactive and neuroprotective steroids occurs in women smokers, and this plays an important role in the activity of the central nervous system, cognition, mental condition, and degree of substance dependence. METHODS: We monitored the effect of smoking discontinuation on steroid spectrum in 40 premenopausal women heavy smokers. These women were examined before they began to discontinue smoking, and after 6, 12, 24 and 48 weeks of abstinence. In each examination, blood was collected to determine steroid spectrum, LH, FSH, and SHBG; basic anthropometric data were also measured using GC-MS or immunoanalysis. Repeated-measures analysis of variance (ANOVA) model was used for evaluation of the data. RESULTS: Given the small number of women who persisted in not smoking, only the data after 6 weeks could be analyzed. No changes were found in C21 steroids, and a slight increase in androgens occurred after the discontinuation of smoking. CONCLUSION: Chronic smoking causes hyperandrogenism in fertile women; after smoking discontinuation, it increases further. Longer-term monitoring is necessary to show the effect of smoking discontinuation on steroid spectrum.