Introduction: The effects of bariatric surgery on skeletal health raise many concerns. Trabecular bone score (TBS) is obtained through the analysis of lumbar spine dual X-ray absorptiometry (DXA) images and allows an indirect assessment of skeletal microarchitecture (MA). The aim of our study was to evaluate the changes in bone mineral density (BMD) and alterations in bone microarchitecture assessed by TBS in morbidly obese women undergoing Roux-en-Y gastric bypass (RYGB), over a three-year follow-up. Material/Methods: A prospective study of 38 morbidly obese white women, aged 46.3 ± 8.2 years, undergoing RYGB was conducted. Biochemical analyses and DXA scans with TBS evaluation were performed before and at one year and three years after surgery. Results: Patients showed normal calcium and phosphorus plasma concentrations throughout the study. However, 25-hydroxyvitamin D (25(OH)D3) decreased, and 71% of patients had a vitamin D deficiency at three years. BMD at femoral neck and lumbar spine (LSBMD) significantly decreased 13.53 ± 5.42% and 6.03 ± 6.79%, respectively, during the three-year follow-up; however Z-score values remained above those for women of the same age. TBS was within normal ranges at one and three years (1.431 ± 106 and 1.413 ± 85, respectively), and at the end of the study, 73.7% of patients had normal bone MA. TBS at three years correlated inversely with age (r = −0.41, p = 0.010), body fat (r = −0.465, p = 0.004) and greater body fat deposited in trunk (r = −0.48, p = 0.004), and positively with LSBMD (r = 0.433, p = 0.007), fat mass loss (r = 0.438, p = 0.007) and lean mass loss (r = 0.432, p = 0.008). In the regression analysis, TBS remained associated with body fat (β = −0.625, p = 0.031; R2 = 0.47). The fracture risk, calculated by FRAX® (University of Sheffield, Sheffield, UK), with and without adjustment by TBS, was low. Conclusion: Women undergoing RYGB in the mid-term have a preserved bone MA, assessed by TBS.

38Background: Limited evidence suggests that epigenetic mechanisms may partially mediate 39 the adverse effects of air pollution on health. Our aims were to identify new genomic loci 40 showing differential DNA methylation associated with long-term exposure to air pollution 41 and to replicate loci previously identified in other studies. 42Methods: A two-stage epigenome-wide association study was designed: 630 individuals from 43 the REGICOR study were included in the discovery and 454 participants of the EPIC-Italy 44 study in the validation stage. DNA methylation was assessed using the Infinium 45 HumanMethylation450 BeadChip. NOX, NO2, PM10, PM2.5, PMcoarse, traffic intensity and 46 traffic load exposure were measured according to the ESCAPE protocol. A systematic review 47 was undertaken to identify those cytosine-phosphate-guanine (CpGs) associated with air 48 pollution in previous studies and we screened for them in the discovery study. 49Results: In the discovery stage of the epigenome-wide association study, 81 unique CpGs 50 were associated with air pollution (p-value <10 -5 ) but none of them were validated in the 51 replication sample. Furthemore, we identified 12 CpGs in the systematic review showing 52 differential methylation with a p-value fulfilling the Bonferroni criteria and 1642 CpGs 53 fulfilling the false discovery rate criteria, all of which were related to PM 2.5 or NO 2 . None of 54 them was replicated in the discovery study, in which the top hits were located in an intergenic 55 region on chromosome 1 (cg10893043, p-value=6.79·10 -5 ) and in the PXK and ARSA genes 56 (cg16560256, p-value=2.23·10 -04 ; cg11953250, p-value=3.64·10 -04 ). 57 Conclusions: Neither new genomic loci associated with long-term air pollution were 58 identified, nor previously identified loci were replicated. Continued efforts to test this 59 potential association are warranted.60 61 BACKGROUND 63Exposure to air pollution remains a global threat with more than 90% of the world's 64 population now exceeding the exposure limits proposed for particulate matter by the World 65 Health Organization (WHO) (1). At the same time, a growing body of evidence consistently 66 supports the adverse health effects of air pollution, which the same WHO report estimates to 67 be related with 3 million premature deaths worldwide each year. However, the mechanisms 68 by which air pollution induces these deleterious effects are not completely understood. 69Epigenetics encompasses mechanisms that regulate gene expression without changing the 70 DNA sequence, and may contribute to the relation between air pollution and health. The most 71 studied epigenetic mechanism is DNA methylation, which is heritable but can also be 72 modified by life-style and environmental factors. Recently, several studies have analyzed the 73 association between air pollution and DNA methylation using a genome-wide approach, and 74 have reported numerous loci showing differential methylation related to this exposure (2-10). 75The aims of this study were bot...

No abstract