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Objective: Uridine might be a common link between pathological pathways in diabetes and cardiovascular diseases. This study aimed to investigate the predictive value of plasma uridine for type 2 diabetes (T2D) and T2D with atherosclerosis. Methods: Individuals with T2D and healthy controls (n = 218) were randomly enrolled in a cross-sectional study. Patients with T2D were divided into two groups based on carotid ultrasound: patients with carotid atherosclerosis (CA) (group DCA) and patients without CA (group D). Plasma uridine was determined using HPLC-MS/MS. Correlation and logistic regression analyses were used to analyze the results. Results: Fasting and postprandial uridine were significantly increased in patients with T2D compared with healthy individuals. Logistic regression suggested that fasting and postprandial uridine were independent risk factors for T2D. The receiver operating characteristic (ROC) curve showed that fasting uridine had a predictive value on T2D (95% CI, 0.686-0.863, sensitivity 74.3%, specificity 71.8%). Fasting uridine was positively correlated with LDL-c, FBG, and PBG and negatively correlated with fasting C-peptide (CP-0h) and HOMA-IS. The change in postprandial uridine from fasting baseline (Δuridine) was smaller in T2D patients with CA compared with those without (0.80 (0.04-2.46) vs 2.01 (0.49-3.15), P = 0.010). Δuridine was also associated with T2D with CA and negatively correlated with BMI, CP-0h, and HOMA-IR. Conclusion: Fasting uridine has potential as a predictor of diabetes. Δuridine is closely associated with carotid atherosclerosis in patients with T2D.
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Background: Acupuncture therapy has demonstrated significant efficacy in the treatment of postherpetic neuralgia, effectively alleviating pain intensity and enhancing patients' quality of life. However, the effectiveness of collateral-pricking and bloodletting cupping combined with electroacupuncture in the treatment of postherpetic neuralgia remains a subject of controversy. We aimed to assess the efficacy and safety of collateral-pricking and bloodletting cupping combined with electroacupuncture for postherpetic neuralgia. Methods: We identified relevant randomized controlled trials by conducting a comprehensive search in multiple databases: China National Knowledge Infrastructure, China Biomedical Literature, Wanfang Data, PubMed, Cochrane Central Register of Controlled Trials, Embase, and Web of Science. The outcome included efficacy rate, visual analog scale (VAS)scores and pittsburgh sleep quality index (PSQI) scores. We meticulously assessed the risk of bias in the included trials and performed a meta-analysis. Results: We analyzed 9 randomized controlled trials involving 639 patients. Collateral-pricking and bloodletting cupping combined with electroacupuncture achieved a significantly higher efficacy rate (risk ratio, 1.22 [95% CI, 1.13-1.31]; P < .001), reduced theVAS scores (standardized mean difference, -1.52 [95% CI, -2.26 to -0.79]; P < .001), and improved the PSQI scores (standardized mean difference, -2.31 [95% CI, -3.97 to -0.64]; P = .007) compared with the control groups. The subgroup analysis revealed that the combined treatment of collateral-pricking and bloodletting cupping and electroacupuncture had a significantly higher total effective rate compared with the carbamazepine, electroacupuncture, and pregabalin groups (P < .05). The total efficacy rate of the collateral-pricking and bloodletting cupping combined with electroacupuncture group was superior to that of the control group, irrespective of whether 2 or 3 courses were administered (P < .05). Conclusion: Existing evidence suggests that the combination of collateral-pricking and bloodletting cupping and electroacupuncture demonstrates efficacy in pain relief, improvement of sleep quality, and enhanced therapeutic outcomes for patients with postherpetic neuralgia. However, further validation through large-scale multicenter randomized controlled trials is warranted due to the limited quantity and quality of the included literature in this study.
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Uridine is a pyrimidine nucleoside found in plasma and cerebrospinal fluid with a concentration higher than the other nucleosides. As a simple metabolite, uridine plays a pivotal role in various biological processes. In addition to nucleic acid synthesis, uridine is critical to glycogen synthesis through the formation of uridine diphosphate glucose in which promotes the production of UDP-GlcNAc in the hexosamine biosynthetic pathway and supplies UDP-GlcNAc for O-GlcNAcylation. This process can regulate protein modification and affect its function. Moreover, Uridine has an effect on body temperature and circadian rhythms, which can regulate the metabolic rate and the expression of metabolic genes. Abnormal levels of blood uridine have been found in people with diabetes and obesity, suggesting a link of uridine dysregulation and metabolic disorders. At present, the role of uridine in glucose metabolism and lipid metabolism is controversial, and the mechanism is not clear, but it shows the trend of long-term damage and short-term benefit. Therefore, maintaining uridine homeostasis is essential for maintaining basic functions and normal metabolism. This article summarizes the latest findings about the metabolic effects of uridine and the potential of uridine metabolism as therapeutic target in treatment of metabolic disorders.
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Uridine is a key metabolite used as a substrate for the production of DNA, RNA, and glucose, and it is mainly synthesized in the liver. Currently, it is not known whether uridine levels are altered in the tumor microenvironment of patients with hepatocellular carcinoma (HCC) and whether uridine can be a target for tumor therapy. In this study, the detection of genes associated with de novo uridine synthesis, carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, dihydroorotase (CAD) (n = 115), and dihydroorotate dehydrogenase (DHODH) (n = 115) in HCC tissues through tissue microarrays revealed that the expression of CAD and DHODH was higher in tumor compared with paraneoplastic tissues. Next, we collected tumor tissues from surgically resected HCC patients and the corresponding adjacent non-tumor tissues (n = 46) for LC-MS/MS assays. The results showed that the median and interquartile ranges of uridine content in non-tumor and tumor tissues were 640.36 (504.45-807.43) and 484.22 (311.91-626.73) nmol/g, respectively. These results suggest that uridine metabolism is disturbed in HCC patients. To further investigate whether uridine can be used as a tumor-therapeutic target, a series of high concentrations of uridine were incubated with HCC cells in vitro and in vivo. It was observed that uridine dose-dependently inhibited the proliferation, invasion, and migration of HCC cells by activating the ferroptosis pathway. Overall, these results reveal for the first time the range of uridine content in human HCC tissues and suggest that uridine may be a new target for HCC therapy.