Association between higher triglyceride glucose index and increased risk of osteoarthritis: data from NHANES 2015-2020.

BACKGROUND: The relationship between the triglyceride glucose (TyG) index and osteoarthritis (OA) remains unclear. The objective of this study was to examine potential associations between an elevated TyG index and an increased risk of OA prevalence. METHODS: 3,921 participants with OA from the National Health and Nutrition Examination Survey (2015-2020) were included in this study. Participants were categorized into quartiles based on TyG index, which was determined using the formula: Ln [triglyceride (mg/dL) fasting blood glucose (mg/dL)/2]. Weighted multivariable regression, subgroup analyses, and threshold effect analyses were performed to calculate the independent association between TyG index and OA. RESULTS: A total of 25,514 people were enrolled, with a mean TyG index of 8.48 ± 0.65. The results of multivariable logistic regression analysis after full adjustment showed a significant association between higher TyG index values and an increased risk of OA. Specifically, each incremental unit increase in the TyG index was associated with a 634% higher risk of OA [OR = 7.34; 95% CI: 2.25, 23.93; p = 0.0010]. Based on interaction tests, age, gender, BMI, and smoking status did not significantly affect the relationship between the TyG index and OA, while diabetes showed a stronger positive correlation between the TyG index and OA. CONCLUSION: An increased risk of OA was associated with a higher TyG index. TyG could be a valuable predictor of OA and offer novel perspectives on the assessment and treatment of OA.

Association between lipid accumulation products and osteoarthritis among adults in the United States: A cross-sectional study, NHANES 2017-2020.

OBJECTIVE: Using cross-sectional data from the 2017-2020 National Health and Nutrition Examination Survey (NHANES) for American, the aim of this research is to investigate the potential association between Lipid Accumulation Products (LAP) and the risk of osteoarthritis (OA). METHODS: Data from the NHANES (2017-2020) were downloaded and further analyzed. The participants between 20 and 80 years reported having OA, and other relevant variables and information on LAP were included. The linear and non-linear associations between LAP and OA were evaluated using multivariable logistic regression analysis and smoothed curve fitting methods. A two-part linear regression model was also used to estimate threshold effects. RESULTS: The increased risk of OA was shown to have a nonlinear relationship with higher LAP, showing a solid threshold impact with a saturation value of 120.00 cm × mmol/L, according to our data. The two variables showed a positive relationship to the left of the saturation point but no significant association to the right, pointing to a complicated nonlinear relationship between OA prevalence and LAP. CONCLUSIONS: Our findings revealed that LAP was an independent risk factor for OA when it was <120.00 cm × mmol/L. The LAP index may serve as a valuable method for predicting and diagnosed OA. To validate our results, further large-scale prospective research are required.

miR-124-3p sabotages lncRNA MALAT1 stability to repress chondrocyte pyroptosis and relieve cartilage injury in osteoarthritis.

BACKGROUND: Osteoarthritis (OA) is a prevalent inflammatory joint disorder. microRNAs (miRNAs) are increasingly involved in OA. AIM: Our study is proposed to clarify the role of miR-124-3p in chondrocyte pyroptosis and cartilage injury in OA. METHODS: OA mouse model was established via the treatment of destabilization of the medial meniscus (DMM), and the in vitro cell model was also established as mouse chondrocytes were induced by lipopolysaccharide (LPS). Mouse cartilage injury was assessed using safranin-O-fast green staining, hematoxylin-eosin staining, and OARSI grading method. Expressions of miR-124-3p, MALAT1, KLF5, and CXCL11 were determined. Cartilage injury (MMP-13, osteocalcin), inflammation (IL-6, IL-2, TNF-, IL-1ß, and IL-18)- and pyroptosis-related factors (Cleaved Caspase-1 and GSDMD-N) levels were detected. Mechanically, MALAT1 subcellular localization was confirmed. The binding relationships of miR-124-3p and MALAT1 and MALAT1 and KLF5 were verified. MALAT1 half-life period was detected. Then, miR-124-3p was overexpressed using agomiR-124-3p to perform the rescue experiments with oe-MALAT1 or oe-CXCL11. RESULTS: miR-124-3p was downregulated in DMM mice and LPS-induced chondrocytes where cartilage injury, and increased levels of inflammation- and pyroptosis-related factors were found. miR-124-3p overexpression relieved cartilage injury and repressed chondrocyte pyroptosis. miR-124-3p bounds to MALAT1 to downregulate its stability and expression, and MALAT1 bounds to KLF5 to enhance CXCL11 transcription. Overexpression of MALAT1 or CXCL11 annulled the repressive function of miR-124-3p in chondrocyte pyroptosis. CONCLUSION: miR-124-3p reduced MALAT1 stability and inhibited the binding of MALAT1 and KLF5 to downregulate CXCL11, thereby suppressing chondrocyte pyroptosis and cartilage injury in OA.