Background Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of reproductive, endocrine, and metabolic functions. Vitamin D has an influence on metabolic and reproductive functions. This study was designed to explore the levels of free 25 hydroxycholecalciferol [25(OH)-D] in PCOS patients. We also aimed to clarify the impact of vitamin D supplementation on cardio-metabolic status, androgen profile, and clinical features of PCOS. Results Our results revealed significant lower levels of serum 25(OH)-D in PCOS women compared with healthy controls. Even more importantly, our results reported that 25(OH)-D levels were negatively correlated with cardio-metabolic risk factors, androgenic profile, and clinical features of PCOS. Stepwise multiple linear regression analysis revealed that carotid intima-media thickness (CIMT), fasting serum insulin (FSI), and fasting plasma glucose (FPG) were the main predictors of 25(OH)-D levels among other clinical and laboratory biomarkers. Considering the impact of VD supplementation in the PCOS group, there were significant improvements of cardio-metabolic risks, PCOS phenotype, and androgenic profile. Even more important, these results are associated with increasing 25(OH)-D serum levels after VD supplementations. Logistic regression analysis observed that androstenedione, FSI, and hirsutism score were independent predictors of response to VD supplementation. Conclusion The supplementation of VD for 12 weeks improved the cardio-metabolic and androgenic profiles of PCOS. Furthermore, VD supplementation could be a promising treatment of PCOS and its associated morbidity in PCOS-deficient women. Trial registration NCT04117750

Vitamin D & vitamin D receptor (VDR) signaling play a very crucial role in early embryonic heart development. We construct this case-control study to investigate the association between maternal serum vitamin D level & VDR gene Fok1 polymorphism and risk of congenital heart defects (CHD) in offspring. Fifty mothers who had term neonates with CHD were considered as cases. Fifty age-comparable healthy mothers who had neonates without CHD were contemplated as controls. Maternal serum 25 hydroxyvitamin D [25(OH) D] level was tested using ELISA. Maternal VDR gene Fok1 polymorphism was analyzed using PCR-based RFLP-assay. There was a significant decrease in maternal vitamin D level ( P = 0.002) and a significant increase in vitamin D deficient status ( P = 0.007) among cases when compared to controls. VDR gene Fok1 genotypes distribution frequency were in accordance with Hardy Weinberg equilibrium (HW) among controls. A significant increase in VDR gene Fok1 F/f & f/f genotypes and f allele were observed in cases compared to controls with estimated odds ratio (95% confidence interval) & P -value of 3 (1–8) & P = 0.006, 11 (1–97) & P = 0.01 and 3 (2–6) & P = 0.001 respectively. There was a significant decrease in maternal vitamin D level in neonates with cyanotic CHD ( P = 0.000) compared to those with a cyanotic CHD while there was no significant difference in VDR Fok1 genotype ( P = 0.18) & allele ( P = 0.05) distribution between two groups. We concluded that maternal vitamin D deficiency and VDR gene Fok1 F/f, f/f genotype and f allele were associated with increased risk of CHD in offspring.

No abstract

No abstract

Lipoprotein Lipase (LPL) is known to be a key enzyme for lipid metabolism specifically in an enzymatic glycoprotein which provide tissues without fatty-acids and eliminates triglycerides (TG) by the circulation. Mutations in LPL were proven to cause alteration in fractions within lipoprotein, causing the development of atherosclerosis which predispose to weakening coronary artery disease (CAD) and stroke. We examined the linkage between genetic variant Hind III in LPL on lipoprotein fractions, stroke occurrences and CAD. In this case-control study, we have recruited 315 CAD cases and 205 age-matched controls. A total of 520 genomic DNA was digested with the purified PCR products for restriction fragment length polymorphism with Hind III restriction enzyme. The distribution of genotypes in a decreasing order were TT, 148 (47%), GT 135 (42.9%) and GG 32 (10.2%) in CAD groups of the study while the pattern in controls were GT 91 (44.4%), TT 86 (42%) and GG 28 (13.7%). None of all the allele or genotype frequencies were found to be significant in our study (p greater than 0.05), while the biochemical levels for both TG and LDL-c were shown to be prone in CAD patients when compare with the controls. Furthermore, the occurence of strokes were more in CAD groups vs. controls: 72 (22.9%) vs. 7 (3.4%) [p 0.000]. This could indicate the influence of Hind III variant on plasma lipid levels, and the possibility of considering it a risk factor for atherosclerosis leading to CAD and stroke occurrence.