Objective: Nonalcoholic fatty liver disease (NAFLD) is related to several inflammatory or metabolic diseases. However, findings of previous studies investigating the association between NAFLD and BMD are inconsistent. Only one study reported a potential association between NAFLD and osteoporotic fracture. This study investigated whether NAFLD in older participants (>55 years) was associated with osteoporotic fracture risk.Materials and Methods: This cross-sectional, observational study included 2,695 participants (35.7% men, 614 cases of NAFLD, and 383 fractures). Standardized questionnaires, laboratory tests, and physical and ultrasonic examinations were completed.Results: After adjusting for various factors including serum triglycerides (TG), high-density cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), multivariate logistic regression models revealed a marginal association between NAFLD and osteoporotic fracture risk in men (odds ratio [OR], 1.86; 95% confidence interval [CI], 1.06–3.27; P = 0.030) but no association in women (OR, 1.05; 95% CI, 0.74–1.48; P = 0.800). Further stratified analyses showed a significant association between NAFLD and osteoporotic fracture risk in men without high TG, low HDL-C, and high LDL-C.Conclusions: There was a significant association between NAFLD and osteoporotic fracture risk in older Chinese men, particularly men without dyslipidemia.
Geraniin, an active compound isolated from Geranium sibiricum, was found to inhibit proliferation and induce apoptosis of tumor cells. However, the antimetastatic effects of geraniin remain elusive. Our study found the potential antitumor mechanisms of geraniin through inhibiting the migration and invasion of human osteosarcoma U2OS cells. The western blot, gelatin zymography, and reversed transcription-PCR analysis showed that geraniin suppressed matrix metalloproteinase-9 (MMP-9) expression in a concentration-dependent manner. Geraniin potently suppressed the phosphorylation of extracellular signal regulating kinase (ERK)1/2, phosphatidylinositide-3-kinase (PI3K), and Akt, but did not affect phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase. Furthermore, when transforming growth factor-β1 (TGF-β1) was used as an agonist, geraniin inhibited TGF-β1-mediated cell invasion and upregulation of MMP-9. These results suggested that geraniin inhibited U2OS cell migration and invasion by reducing the expression of MMP-9 through the PI3K/Akt and ERK1/2 signaling pathways.
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