Promoting the browning of white fat may be a potential means of combating obesity. Therefore, in this study, we investigated the effect of resveratrol (RES) on the body weight and browning of white fat in high-fat diet (HFD)-induced obese mice and the potential associated mechanism in vivo. Eight-week-old male mice were randomized to receive different treatments: (1), chow without any additional treatment (chow); (2), chow plus 0.4% resveratrol (chow-RES); (3), HFD without any additional treatment (HFD); and (4), HFD plus 0.4% resveratrol (HFD-RES). After 4 weeks of feeding, additional 8-week-old male recipient mice were randomly allocated to the following 4 treatments: (5), HFD and received feces from chow-fed mice; (6), HFD and received feces from chow-RES-fed mice; (7), HFD and received feces from HFD-fed mice; and (8), HFD and received feces from HFD-RES-fed mice. RES treatment significantly inhibited increases in fat accumulation, promoted the browning of white adipose tissue (WAT) and alleviated gut microbiota dysbiosis in HFD-fed mice. Subsequent analyses showed that the gut microbiota remodeling induced by resveratrol had a positive role in WAT browning, and sirtuin-1 (Sirt1) signaling appears to be a key component of this process. Overall, the results show that RES may serve as a potential intervention to reduce obesity by alleviating dysbiosis of the gut microbiota.

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Background: Browning of white adipose tissues (WAT) is recognized as a novel way to combat obesity and its related comorbidities. Thus, a lot of dietary agents contributing to browning of WAT have been identified. Objective: In this study, we try to explore the mechanism of the browning of WAT induced by resveratrol (Res) in 3T3-L1 adipocytes. Methods: The levels of cell viability and lipid accumulation were evaluated under different concentrations of Res. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the WAT browning effect of Res in 3T3-L1 cells. Results: We found that Res induced the brown fat-like phenotype by activating protein expressions of brown adipocyte-specific markers, such as peroxisome proliferator-activated receptor gamma (PPAR-γ), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), and uncoupling protein 1 (UCP1). Besides, Res reduced lipid accumulation, as shown by Oil Red O staining. The increased small lipid droplets implied that Res-treated 3T3-L1 adipocytes had some features of brown adipocytes. The brown fat-like phenotype in 3T3-L1 adipocytes induced by Res was possibly mediated by activation of mammalian target of rapamycin (mTOR), as brown adipocyte-specific markers were decreased by rapamycin, an inhibitor of mTOR and the MHY1485 treatment, an activator of mTOR, showed the similar effect of Res on browning markers. Conclusions: Res induced brown-like adipocyte phenotype in 3T3-L1 adipocytes partly via mTOR pathway, which provided new insights into the utilization of Res to prevent obesity and related comorbidities.

Lung adenocarcinoma (LUAD) is often diagnosed at an advanced stage, so it is necessary to identify potential biomarkers for the early diagnosis and prognosis of LUAD. In our study, a gene co-expression network was constructed using weighted gene co-expression network analysis (WGCNA) in order to obtain the key modules and genes correlated with LUAD prognosis. Four hub genes (HLF, CHRDL1, SELENBP1, and TMEM163) were screened out using least absolute shrinkage and selection operator (LASSO)–Cox regression analysis; then, a prognostic model was established for predicting overall survival (OS) based on these four hub genes..Furthermore, the prognostic values of this four-gene signature were verified in four validation sets (GSE26939, GSE31210, GSE72094, and TCGA-LUAD) as well as in the GEPIA database. To assess the prognostic values of hub genes, receiver operating characteristic (ROC) curves were constructed and a nomogram was created. We found that a higher expression of four hub genes was associated with a lower risk of patient death. In a training set, it was demonstrated that this four-gene signature was a better prognostic factor than clinical factors such as age and stage of disease. Moreover, our results revealed that these four genes were suppressor factors of LUAD and that their high expression was associated with a lower risk of death. In summary, we demonstrated that this four-gene signature could be a potential prognostic factor for LUAD patients. These findings provide a theoretical basis for exploring potential biomarkers for LUAD prognosis prediction in the future.