Bone mineral density saturation as influenced by the visceral adiposity index in adults older than 20 years: a population-based study.

OBJECTIVE: The goal of this research was to determine whether or not there is a saturation effect and whether or not the visceral adiposity index (VAI) correlates with bone mineral density (BMD) in adult Americans. METHODS: This study used multivariate logistic regression models to examine the association between VAI and total femur BMD, drawing on the most up-to-date data from the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2018. Saturation levels and non-linear connections were calculated using a smooth curve-fitting algorithm and an investigation of saturation effects. Subgroup analyses and interaction tests were also conducted. RESULTS: This study ultimately recruited 6257 individuals aged 20 years or older. According to multivariate regression analysis, those with high VAI scores exhibited higher total femur BMD. Total femur BMD was greater in the highest VAI quartile (Q4: 0.060 g/cm2) after adjustment than in the lowest VAI quartile (Q1) (P < 0.05). After controlling for variables, subgroup analysis failed to reveal any significant interaction effects. Furthermore, the study determined that VAI and BMD exhibited a specific saturation effect through the investigation of the saturation effect and the fitting of smooth curves. Saturation effect investigation of total femur BMD using VAI revealed a saturation value of 3.3. CONCLUSION: The present study uncovered a non-linear relationship between VAI and total femur BMD, which exhibited a saturation effect.

Cinnamaldehyde Alleviates Bone Loss by Targeting Oxidative Stress and Mitochondrial Damage via the Nrf2/HO-1 Pathway in BMSCs and Ovariectomized Mice.

Osteoporosis (OP) is typically brought on by disruption of bone homeostasis. Excessive oxidative stress and mitochondrial dysfunction are believed to be the primary mechanisms underlying this disorder. Therefore, in order to restore bone homeostasis effectively, targeted treatment of oxidative stress and mitochondrial dysfunction is necessary. Cinnamaldehyde (CIN), a small molecule that acts as an agonist for the nuclear factor erythroid 2-related factor (Nrf2), has been found to possess antiapoptotic, anti-inflammatory, and antioxidant properties. We found that CIN, while rescuing apoptosis, can also reduce the accumulation of reactive oxygen species (ROS) to improve mitochondrial dysfunction and thus restore the osteogenic differentiation potential of BMSCs disrupted by hydrogen peroxide (H2O2) exposure. The role of CIN was preliminarily considered to be a consequence of Nrf2/HO-1 axis activation. The ovariectomized mice model further demonstrated that CIN treatment ameliorated oxidative stress in vivo, partially reversing OVX-induced bone loss. This improvement was seen in the trabecular microarchitecture and bone biochemical indices. However, when ML385 was concurrently injected with CIN, the positive effects of CIN were largely blocked. In conclusion, this study sheds light on the intrinsic mechanisms by which CIN regulates BMSCs and highlights the potential therapeutic applications of these findings in the treatment of osteoporosis.