Association between Oral vitamin C supplementation and serum uric acid: A meta-analysis of randomized controlled trials.

INTRODUCTION: Results from recent trials assessing the effect of oral vitamin C supplementation on serum uric acid (SUA) have been inconsistent. OBJECTIVES: The purpose of this study was to explore the association between oral vitamin C supplementation and serum uric acid. METHODS: PUBMED, EMBASE, CNKI, Web of Science, and CENTRAL of Cochrane library databases were searched to identify relevant articles published up to February 2020. Heterogeneity was evaluated using I-square (I2) statistics. Random-effects model was used to pool weighted mean differences (WMD) and 95 % confidence interval (CI) as summary effect sizes. RESULTS: The total sixteen eligible randomized controlled trials (RCTs) containing 1,013 participants were included in this meta-analysis. The pooled findings showed that vitamin C supplementation had a significant effect of lowering SUA. The subgroup analyses showed that the effect of vitamin C supplementation on SUA has positive association with mean age of participants <65 years old, the use of placebo or blank control, duration of trials <1 month and high-quality studies. In addition, sensitivity analysis showed that the results of this study were stable. Both Egger's test and Begg's test demonstrated that no evidence of significant publication bias. CONCLUSIONS: The results of present meta-analysis have demonstrated that vitamin C supplementation could make a reduction of SUA. The use of placebo, duration of intervention, age of the subjects and study quality have an impact on the effect of oral vitamin C, but the baseline of SUA not.

Timosaponin B-II Ameliorates Palmitate-Induced Insulin Resistance and Inflammation via IRS-1/PI3K/Akt and IKK/NF-[Formula: see text]B Pathways.

This study aimed to investigate the effect of timosaponin B-II (TB-II) on palmitate (PA)-induced insulin resistance and inflammation in HepG2 cells, and probe the potential mechanisms. TB-II, a main ingredient of the traditional Chinese medicine Anemarrhena asphodeloides Bunge, notably ameliorated PA-induced insulin resistance and inflammation, and significantly improved cell viability, decreased PA-induced production of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]) and interleukin-6 (IL-6) levels. Further, TB-II treatment notably decreased malondialdehyde (MDA) and lactate dehydrogenase (LDH) levels, and improved superoxide dismutase (SOD) and nitric oxide (NO). TB-II also reduced HepG2 cells apoptosis. Insulin receptor substrate-1 (IRS1)/phosphatidylinositol 3-kinase (PI3K)/Akt and inhibitor of nuclear factor [Formula: see text]-B kinase (IKK)/NF-[Formula: see text]B pathways-related proteins, and IKK[Formula: see text], p65 phosphorylation, serine phosphorylation of insulin receptor substrate-1 (IRS-1) at S307, tyrosine phosphorylation of IRS-1, and Akt activation were determined by Western blot. Compared to model group, TB-II significantly downregulated the expression of p-NF-[Formula: see text]Bp65, p-IKK[Formula: see text], p-IRS-1, p-PI3K and p-Akt. TB-II is a promising potential agent for the management of palmitate-induced insulin resistance and inflammation, which might be via IR/IRS-1/PI3K/Akt and IKK/NF-[Formula: see text]B pathways.