ABSTRACT. We conducted a case-control study to investigate the role of three common polymorphisms (rs10754558, rs7512998, and rs12137901) of the gene NLR family, pyrin domain containing 3 (NLRP3) in the development of type 2 diabetes mellitus (T2DM). Between May 2013 and May 2014, 385 patients with T2DM and 401 control subjects were enrolled in our study. Genotyping of the three NLRP3 polymorphisms of interest was performed by polymerase chain reaction-restriction fragment length polymorphism. Unconditional logistic regression analyses showed that individuals carrying GG and GC+GG rs10754558 genotypes were at significantly increased risk of T2DM, with adjusted odds ratios (and 95% confidence intervals) of 1.81 (1.16-2.83) and 1.40 (1.04-1.88), respectively. In conclusion, we propose that the NLRP3 rs10754558 polymorphism contributes to the development of T2DM, but that rs7512998 and rs12137901 variants are not associated with susceptibility to this disease.

ABSTRACT. Coronary artery disease (CAD) represents a leading cause of morbidity and mortality worldwide, and genetic factors contribute to the development of this disease. We conducted a case-control study to assess the association between interleukin 17A (IL17A) rs2275913 and rs3748067 polymorphisms and development of CAD. A total of 372 CAD patients and 372 healthy controls were recruited in our investigation between January 2013 and December 2014. Genotyping of IL17A rs2275913 and rs3748067 was carried out using polymerase chain reaction combined with restriction fragment length polymorphism. Logistic regression analysis revealed that CC [odds ratio (OR) = 3.81, 95% confidence interval (CI) = 2.11-7.16] and TC+CC (OR = 1.54, 95%CI = 1.11-2.14) rs3748067 genotypes were associated with an increased risk of CAD compared to the TT variant. Individuals carrying the TC+CC genotype were more likely to have a higher risk of CAD if they were smokers, with an adjusted OR (and 95%CI) of 2.20 (1.31-3.71). In conclusion, we suggest that the CC and TC+CC genotypes

Introduction In the aging process of the body, in addition to changes in fat and muscle content, there is also bone loss, implying the possibility of a strong muscle–bone–lipid link. In this study, we initially investigated the relationship between lumbar BMD and low muscle mass and the relationship between “muscle–bone–lipid.” Methods The datasets from the National Health and Nutrition Examination Survey (NHANES) 2011–2018 were used in a cross-sectional investigation. BMD and appendicular skeletal muscle (ASM) were measured by dual-energy X-ray absorptiometry (DXA), and appendicular skeletal muscle was adjusted by body mass index (BMI) as a marker of sarcopenia. Weighted multivariate regression and logistic regression analysis were used to explore the independent relationship between lumbar BMD and sarcopenia. Fitted smoothing curves and threshold effect analysis were used to describe the nonlinear relationship. Result In 8386 participants with ages 20–59 years, there was a negative association between lumbar BMD and sarcopenia. In the fully adjusted model, the risk of developing sarcopenia decreased by 93% for each 1-unit increase in lumbar BMD (OR = 0.07, 95%CI 0.03–0.20). The risk of sarcopenia was 58% lower in participants in the highest quartile of lumbar BMD than in those in the lowest quartile (OR = 0.42, 95%CI 0.27–0.64). This negative association was more pronounced in the population of women with BMI ≥ 25. Conclusion Our findings suggest that lumbar BMD is negatively associated with sarcopenia in US adults. The dynamic balance between “muscle–bone–lipid” is likely to be related to the pathogenesis of bone loss.

Background Type 2 diabetes mellitus (DM2) and osteoporosis (OP) are currently the two most significant causes of mortality and morbidity in older adults, according to clinical evidence. The intrinsic link between them is yet unknown, despite reports of their coexistence. By utilizing the two-sample Mendelian randomization (MR) approach, we sought to evaluate the causal impact of DM2 on OP. Methods The aggregate data of the whole gene-wide association study (GWAS) were analyzed. A two-sample MR analysis was performed using single-nucleotide polymorphisms (SNPs), which are strongly associated with DM2, as instrumental variables (IVs) to evaluate the causal analysis of DM2 on OP risk with OR values, using inverse variance weighting, MR-egger regression, and weighted median methods, respectively. Result A total of 38 single nucleotide polymorphisms were included as tool variables. According to the results of inverse variance-weighted (IVW), we found that there was a causal relationship between DM2 and OP, in which DM2 had a protective effect on OP. For each additional case of DM2, there is a 0.15% decrease in the odds of developing OP (OR = 0.9985;95%confidence interval:0.9974,0.9995; P value = 0.0056). There was no evidence that the observed causal effect between DM2 and the risk of OP was affected by genetic pleiotropy (P = 0.299). Using Cochran Q statistics and MR-Egger regression in the IVW approach, the heterogeneity was calculated; P > 0.05 shows that there is a significant amount of heterogeneity. Conclusion A causal link between DM2 and OP was established by MR analysis, which also revealed that DM2 decreased the occurrence of OP.