Background: Osteoporosis, a systemic skeletal disease characterized by low bone mass and increased fracture risk, poses significant social and economic challenges globally, while type 2 diabetes mellitus (T2DM), a prevalent metabolic disorder, has been linked to complex effects on bone health, including contradictory findings on its relationship with osteoporosis and fracture risk. Methods: We searched PubMed, Embase, Cochrane, and Web of Science Library to identify observational studies investigating whether people with T2DM have a higher risk of osteoporosis or fracture than people without diabetes. The time limit for literature retrieval was from the establishment of the database until March 2023. The quality of the studies was assessed using the Newcastle-Ottawa Scale and Agency for Healthcare Research and Quality checklist. The meta-analysis was conducted using Stata 15, and a random-effects model was used if I² was > 50%. The Egger test was used to assess publication bias. Results: The results demonstrated that people with T2DM have a higher risk of osteoporosis. (relative risk, 1.841; 95% confidence interval, 1.219–2.780; P = .004). Similar results were demonstrated for fractures (relative risk, 1.21; 95% confidence interval, 1.09–1.31; P < .001). However, the results of the subgroup analysis showed no significant correlation between T2DM and fractures in univariate analysis, cross-sectional studies, Asia, Europe, Oceania, and vertebral fractures. However, a significant correlation was found in other subgroup analyses. Conclusions: Osteoporosis and fractures are significantly associated with T2DM.

Steroid-induced osteonecrosis of the femoral head (SONFH) is a prevalent refractory condition in orthopedics, often causing high disability rates. Gu Fu Sheng Capsule (GFSC) is commonly used to treat SONFH during the early and intermediate stages. However, the precise underlying mechanism of action of GFSC remains elusive. To elucidate the mechanism through which GFSC improves lipid metabolism in rats with SONFH. A rat model of SONFH was established by administering methylprednisolone and lipopolysaccharide. Micro-computed tomography assessed femoral head effects, while hematoxylin–eosin staining examined femoral head tissues. Pathological changes were evaluated using an automated biochemical analyzer to measure changes in serum lipid levels. Besides, quantitative lipidomics and network pharmacology were used to determine how GFSC impacts SONFH. qRT-PCR and Western blotting were performed to assess mRNA and protein expression levels of key targets. GFSC can enhance bone density and prevents surface collapse of the femoral head, improve hollow bone lacuna density, reduce adipocyte infiltration, minimize osteocyte cavities, regulate the serum lipid levels and enhance lipid metabolism in SONFH rats. Moreover, integrated lipidomics and network pharmacology suggested that GFSC affects lipid metabolism-related genes by regulating nine targets, thereby influencing four metabolites and two metabolic pathways, which may mainly be due to components in GFSC such as quercetin, tanshinone iia, berberine. Western blotting and qRT-PCR data highlighted that GFSC improves lipid metabolism by regulating TP53, HSP90AA1, and ESR1. GFSC effectively retards SONFH progression, potentially attributed to its ability to regulate lipid metabolism.

Objective. This study is aimed at investigating the expression of Met and YAP in gastric cancer and their impact on clinical prognosis. Methods. Tissue samples and clinical data were collected from 89 patients with gastric cancer. Immunohistochemistry was performed to quantify the expression of Met and YAP using tissue microarray. The correlation between the expressions of Met, YAP, and clinicopathological characteristics of patients was determined using a chi‐square test. Survival analysis was conducted using the Kaplan‐Meier method, while multivariate survival analysis was performed using the Cox proportional hazard model. Bioinformatics analysis was carried out by downloading chip data from TCGA. Results. The expression levels of both Met and YAP were significantly higher in gastric cancer tissues compared to adjacent tissues (P < 0.001). Met expression showed a positive association with P53 and CD133, whereas YAP expression correlated positively with tumor grade and CD133 (P < 0.05). Pearson’s analysis revealed a significant correlation between Met expression and VEGFR as well as CD133, while YAP expression correlated with Ki67 and VEGFR (P < 0.05). Patients with high levels of both Met and YAP exhibited decreased survival time (P < 0.01). Furthermore, Met expression, N stage, and VEGFR were identified as independent risk factors for gastric cancer prognosis (P < 0.05), whereas no such association was observed for YAP expression. Bioinformatics analysis demonstrated a significant correlation between the expressions of Met and YAP; both proteins were highly expressed in gastric cancer patients accompanied by markedly reduced survival time. Conclusion. The expressions of Met and YAP are closely associated with the survival outcomes as well as clinicopathological features in patients with gastric cancer. Moreover, our findings highlight that Met serves as an independent prognostic factor for gastric cancer.