Vanadium compounds were identified to be beneficial for the control of glucose homeostasis. We aimed to explore the association of plasma vanadium (V) with gestational diabetes mellitus (GDM). We performed a case-control study including 252 newly diagnosed GDM cases and 252 controls matched by age, parity, and gestational age. Fasting blood samples were collected from each participant at GDM screening (≥24 weeks of gestation). The plasma concentrations of V were determined utilizing inductively coupled plasma mass spectrometry. Plasma V levels were significantly lower in the GDM group than those in the control group (p < 0.001). The adjusted OR (95% CI) of GDM comparing the highest V tertile with the lowest tertile was 0.35 (0.20–0.61). According to the cubic spline model, the relation between plasma V and odds of GDM was potentially nonlinear (p < 0.001). Moreover, plasma V was negatively correlated with 1-h post-glucose load, 2-h post-glucose load, and lipid metabolism indices (all p < 0.05). The present study indicates an inverse association of plasma V with GDM. Further prospective cohort studies are required to validate our results.

Plasma transthyretin may be engaged in glucose regulation. We aimed to investigate the association between plasma transthyretin levels and the risk of newly diagnosed T2DM and impaired glucose regulation (IGR) in a Chinese population. We conducted a case-control study including 1244 newly diagnosed T2DM patients, 837 newly diagnosed IGR patients, and 1244 individuals with normal glucose tolerance (NGT) matched by sex and age. Multivariate logistic regression analysis was utilized to estimate the independent association of plasma transthyretin concentrations with the risk of T2DM and IGR. Plasma transthyretin concentrations were significantly higher in T2DM and IGR patients compared with control subjects (p < 0.005). After multiple adjustment and comparison with the lowest quartile of plasma transthyretin concentrations, the odds ratios (95% confidence intervals) of T2DM and IGR in the highest quartile were 2.22 (1.66, 2.98) and 2.29 (1.72, 3.05), respectively. Plasma transthyretin concentrations also showed a great performance in predicting the risk of T2DM (AUC: 0.76). Moreover, a potential nonlinear trend was observed. Our results demonstrated that higher plasma transthyretin concentrations, especially more than 290 mg/L, were associated with an increased risk of T2DM and IGR. Further studies are warranted to confirm our findings and elucidate the potential mechanisms.

Background: Advanced glycation end products (AGEs), a group of food processing byproducts, have been implicated in the development of various diseases. However, the relationship between circulating AGEs and sleep disorders remains uncertain. Methods: This cross-sectional study elucidated the association of plasma AGEs with sleep disorders among 1732 Chinese adults who participated in the initial visit (2019–2020) of the Tongji–Shenzhen Cohort (TJSZC). Sleep behavior was assessed using self-reported questionnaires and precise accelerometers. Plasma levels of AGEs, including Nε-(Carboxymethyl)lysine (CML), Nε-(Carboxyethyl)lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolone-2-yl)-ornithine (MG-H1), were quantified by ultra-high performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS). Results: In logistic regression, per IQR increment in individual AGEs was associated with an increased odds ratio of short sleep duration (CML: 1.11 [1.00, 1.23]; CEL: 1.16, [1.04, 1.30]), poor sleep quality (CML: 1.33 [1.10, 1.60]; CEL: 1.53, [1.17, 2.00]; MG-H1: 1.61 [1.25, 2.07]), excessive daytime sleepiness (CML: 1.33 [1.11, 1.60]; MG-H1: 1.39 [1.09, 1.77]), and insomnia (CML: 1.29 [1.05, 1.59]). Furthermore, in weighted quantile sum regression and Bayesian kernel machine regression analyses, elevated overall exposure levels of plasma AGEs were associated with an increased risk of sleep disorders, including short sleep duration, poor sleep quality, excessive daytime sleepiness, and insomnia, with CML being identified as the leading contributor. Insufficient vegetable intake and higher dietary fat intake was associated with an increase in plasma CEL. Conclusions: These findings support a significant association between plasma AGEs and sleep disorders, indicating that AGEs may adversely influence sleep health and reducing the intake of AGEs may facilitate preventing and ameliorating sleep disorders.

Background: Bisphenol F (BPF), a widely used bisphenol A substitute and emerging endocrine disruptor, has been implicated in bone loss; however, its underlying mechanisms remain unclear. Curcumin (CUR) has shown beneficial effects on bone metabolism, but its protective role against BPF-induced osteogenic impairment requires further validation. This study investigated the involvement of the PI3K/AKT signaling pathway in BPF-induced osteoporosis and osteogenic dysfunction, and whether CUR could alleviate these effects through modulation of this pathway. Methods: Network toxicology, network pharmacology, and molecular docking were first used to predict potential targets and signaling pathways. A rat model of BPF-induced osteoporosis and a BPF-treated MC3T3-E1 osteogenic impairment model were then established to evaluate the effects of CUR. Bone mineral density, trabecular microarchitecture, serum bone metabolism markers, and osteogenic protein expression were assessed in vivo. In vitro, alkaline phosphatase activity, mineralization, and key signaling proteins were measured. The PI3K/AKT inhibitor LY294002 was used to verify pathway involvement. Results: Computational analyses suggested that BPF and CUR were closely associated with the PI3K/AKT pathway. Experimentally, BPF reduced bone mass, disrupted trabecular structure, and suppressed osteogenic differentiation, accompanied by downregulation of osteogenic markers and PI3K/AKT signaling. Notably, BPF reduced femoral BMD by 10.8%, whereas CUR restored approximately 43.5% of the BPF-induced loss. CUR significantly reversed these effects, whereas LY294002 abolished the protective actions of CUR. Conclusions: BPF may impair bone formation and promote osteoporosis by suppressing PI3K/AKT signaling, while CUR alleviates these effects through pathway activation. These findings provide mechanistic evidence supporting CUR as a potential intervention against BPF-related bone toxicity.