Gut microbiome:Linking together obesity,bariatric surgery and associated clinical outcomes under a single focus

Obesity is increasingly prevalent in the post-industrial era,with increased mortality rates.The gut microbiota has a central role in immunological,nutritional and metabolism mediated functions,and due to its multiplexity,it is considered an independent organ.Modern high-throughput sequencing techniques have allowed phylogenetic exploration and quantitative analyses of gut microbiome and improved our current understanding of the gut microbiota in health and disease.Its role in obesity and its changes following bariatric surgery have been highlighted in several studies.According to current literature,obesity is linked to a particular microbiota profile that grants the host an augmented potential for calorie release,while limited diversity of gut microbiome has also been observed.Moreover,bariatric surgery procedures represent effective interventions for sustained weight loss and restore a healthier microbiota,contributing to the observed fat mass reduction and lean mass increase.However,newer evidence has shown that gut microbiota is only partially recovered following bariatric surgery.Moreover,several targets including FGF15/19(a gutderived peptide),could be responsible for the favorable metabolic changes of bariatric surgery.More randomized controlled trials and larger prospective studies that include well-defined cohorts are required to better identify associations between gut microbiota,obesity,and bariatric surgery.

Microglial Exosome miR-7239-3p Promotes Glioma Progression by Regulating Circadian Genes

Glioma-associated microglial cells,a key component of the tumor microenvironment,play an important role in glioma progression.In this study,the mouse glioma cell line GL261 and the mouse microglia cell line BV2 were chosen.First,circadian gene expression in glioma cells co-cultured with either M1 or M2 microglia was assessed and the exosomes of M2-polarized and unpolarized BV-2 microglia were extracted.Subsequently,we labeled the exosomes with PKH67 and treated GL261 cells with them to investigate the exosome distribution.GL261 cell phenotypes and related protein expression were used to explore the role of M2 microglial exosomes in gliomas.Then a specific miR-7239-3p inhibitor was added to verify miR-7239-3p functions.Finally,the mouse subcutaneous tumorigenic model was used to verify the tumorigenic effect of M2 microglial exosomes in vivo.Our results showed that in gliomas co-cultured with M2 microglia,the expression of the BMAL1 protein was decreased(P<0.01),while the expression of the CLOCK protein was increased(P<0.05);opposite results were obtained in gliomas co-cultured with M1 microglia.After treatment with M2 microglial exosomes,the apoptosis of GL261 cells decreased(P<0.001),while the viability,proliferation,and migration of GL261 cells increased.Increased expression of N-cadherin and Vimentin,and decreased E-cadherin expression occurred upon treatment with M2 microglial exosomes.Addition of an miR-7239-3p inhibitor to M2 microglial exosomes reversed these results.In summary,we found that miR-7239-3p in the glioma microenvironment is recruited to glioma cells by exosomes and inhibits Bmal1 expression.M2 microglial exosomes promote the proliferation and migration of gliomas by regulating tumor-related protein expression and reducing apoptosis.