The association between alcohol intake and the risk of glioma has been widely studied, but these results have yielded conflicting findings. Therefore, we conducted this systematic review and updated meta-analysis to systematically evaluate the association between alcohol intake and the risk of glioma. A systematic literature search of relevant articles published in PubMed, Web of Science, CNKI and Wan fang databases up to December 2021 was conducted. Pooled estimated of relative risk(RR) and 95% confidence interval(CI) were calculated using fixed-effects models. A total of eight articles with three case-control studies involving 2706 glioma cases and 2189927 participants were included in this meta-analysis.A reduced risk of glioma was shown for the low-moderate alcohol drinking versus non-drinking(RR=0.87; 95%CI: 0.78, 0.97; P=0.014). In addition, there was no evidence of an increased risk of glioma in the heavy alcohol drinking compared with non-drinking (RR=0.89; 95%CI: 0.67, 1.18; P=0.404). The findings suggest an inverse association between low-moderate alcohol drinking and the risk of glioma, in the absence, however, of a dose-response relationship. More prospective studies are needed to provide further insight into the association between alcohol drinking and glioma risk.

Lipoxin A4 (LXA4) promotes the browning of white adipose and energy consumption. The specific mechanism of which involved in white adipose browning is less clear. A high-fat diet (HFD) mouse model was constructed. Different groups of mice were treated with LXA4 accordingly. The body weight of mouse, subcutaneous and visceral fat, and food intake were recorded. The effect of LXA4 was examined by observing changes in pathology, serum insulin and lipid accumulation indices. The effects of LXA4/miR-133a-3p/Sirtuin1 on lipid droplet formation, fat browning-related genes, and the insulin receptor-AKT pathway in cells were examined after induction of adipocyte differentiation in 3T3-L1 precursors. At the cellular level, LXA4 promoted lipid droplet formation, expressions of fat browning genes and activation of the insulin receptor-AKT pathway in differentiated 3T3-L1 cells. MiR-133a-3p agomir partially offset the effects of LXA4. SIRT1 was a downstream target gene of miR-133a-3p, participating in the promotive effects of LXA4 on fat browning. LXA4 promotes white adipose browning and relieves insulin resistance through miR-133a-3p/SIRT1 pathway.

Given the established positive role of Lipoxin A4 (LXA4) in adipose browning at the cellular level, this study investigated its possible effect on white fat browning and the underlying molecular mechanisms. The obese insulin resistance mouse model was established. The body weight, subcutaneous and visceral fat, and food intake of the mice were observed. Haematoxylin-eosin staining was used to determine the effects of LXA4 on the morphology of inguinal white adipose tissue and brown adipose tissue, and to analyse the changes in fat mass and serum insulin levels, lipid metabolism and other indexes. The cellular experiments included the induction of browning in 3T3-L1 precursor adipocytes, the screening of miRNAs related to adipose browning and their downstream target genes using TargetScan, qRT-PCR, RNA immunoprecipitation and dual luciferase reporter assay. LXA4 attenuated weight gain, inhibited fat accumulation, and improved hyperlipidaemia and insulin resistance in high-fat diet-treated mice. LXA4 also promoted browning of 3T3-L1 precursor adipocytes. Activation of miR-133a-3p partially abrogated LXA4-induced promotion of white adipose browning. The effects of LXA4 and miR-133a-3p could be reversed by SIRT1. Collectively, LXA4 alleviates obesity-related metabolic disorders by promoting inguinal white adipose browning and improving insulin resistance possibly through the miR-133a-3p/SIRT1 pathway.