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Although it is well known dietary factors are closely correlated with bone health, the association between macronutrients intake distribution and bone mineral density (BMD) is still unclear. The aims of this study were to investigate how macronutrients distribution was correlated with BMD, and to evaluate how the substitution between macronutrients could be associated with BMD. We conducted a cross-sectional study based on data from National Health and Nutrition Examination Survey. Dietary recall method was used to assessed the intake of macronutrients. Macronutrient intake distribution including carbohydrate, protein and fat was calculated as percentages of energy intake from total energy. BMD was converted to T-score and low BMD was defined as T-score less than −1.0. The association between the percentages of energy intake from carbohydrate, protein and fat with T-score and risk of low BMD was evaluated using multivariate regression models. Isocaloric substitution analysis was conducted using the multivariate nutrient density method. Data form 4447 adults aged 20 years and older who underwent BMD examination were included in this study. Higher percentage of energy intake from carbohydrate was associated with lower T-score (−0.03 [95%CI, −0.05 to −0.01]; P = 0.001) and higher risk of low BMD (1.05 [95%CI, 1.02–1.08]; P = 0.003), while higher percentage of energy intake from protein was associated with higher T-score (0.05 [95%CI, 0.01–0.08]; P = 0.009) and lower odds of low BMD (0.92 [95%CI, 0.87–0.98]; P = 0.007). The percentage of energy intake from fat seemed to be positively correlated with T-score, but the correlation became insignificant after adjusting for metabolism related confounders. Isocaloric substitution analysis showed that only the substitution between carbohydrate and protein was significantly and independently associated with T-score (−0.05 [95%CI, −0.08 to −0.01]; P = 0.01) and the risk of low BMD (1.08 [95%CI, 1.02–1.15]; P = 0.008). Based on the results from this study, we hypothesized that a high-protein diet coupled with low carbohydrate intake would be beneficiary for prevention of bone loss in adults. However, randomized clinical trials or longitudinal studies are needed to further assessed our findings. [ABSTRACT FROM AUTHOR]

1-nitropyrene (1-NP) is representative nitropolycyclic aromatic hydrocarbon pollutant widely present in exhaust particles of internal combustion engine, which is known for its carcinogenicity and mutagenicity. Previous studies have demonstrated that 1-NP has reproductive toxicity, but the specific mechanism is unknown. In this study, Human decidual stromal cells (HDSCs) were treated by 1-NP, exosomes were extracted from the conditioned medium of HDSCs, which were then used to treat human chorionic trophoblast cells (HTR8/SVneo) for 24 h. The findings showed that human decidual stromal cell-derived exosomes (HDSC-EXOs) can promote the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT; Vimentin and N-cadherin) of HTR8/SVneo by about 64%, 17%, 23%, 81% and 13%. The process of regulating the biological behaviors of embryonic trophoblast cells by maternal decidual stromal cells during pregnancy was simulated. Further investigations showed that HDSC-EXOs treatment activated the Wnt/β-catenin signaling pathway in HTR8/SVneo. Co-treatment by dickkopf-1 (DKK-1) significantly suppressed the activation of Wnt/β-catenin signaling pathway in HTR8/SVneo, and inhibited the proliferation, migration, invasion and EMT (N-cadherin and E-cadherin) of HTR8/SVneo by about 60%, 22%, 42%, 25%, 55% and 21%. These findings indicated that 1-NP exposure could induce the secretion of HDSC-EXOs from HDSCs, which in turn activate the Wnt/β-catenin signaling pathway and enhance the proliferation, migration, invasion and EMT of HTR8/SVneo. [Display omitted] • 1-NP exposure could induce the secretion of HDSC-EXOs from HDSCs. • HDSC-EXOs can activate the Wnt/β-catenin signaling pathway. • HDSC-EXOs can promote the malignant biological behavior and EMT of HTR8/SVneo. [ABSTRACT FROM AUTHOR]