Recent studies have investigated the anti-obesity effect of resveratrol, but the pathways through which resveratrol resists obesity are not clear. In the present study, we hypothesize that resveratrol exerts anti-obesity effects that are likely mediated by mechanisms of regulating gut microbes, and in turn, improving fat storage and metabolism. Gut microbes, glucose and lipid metabolism in high-fat diet (HF) mice in vivo are investigated after resveratrol treatment. Several biochemical markers are measured. Fluorescence in situ hybridization and flow cytometry are used to monitor and quantify the changes in gut microbiota. The key genes related to fat storage and metabolism in the liver and visceral adipose tissues are measured by real-time PCR. The results show that resveratrol (200 mg per kg per day) significantly lowers both body and visceral adipose weights, and reduces blood glucose and lipid levels in HF mice. Resveratrol improves the gut microbiota dysbiosis induced by the HF diet, including increasing the Bacteroidetes-to-Firmicutes ratios, significantly inhibiting the growth of Enterococcus faecalis, and increasing the growth of Lactobacillus and Bifidobacterium. Furthermore, resveratrol significantly increases the fasting-induced adipose factor (Fiaf, a key gene negatively regulated by intestinal microbes) expression in the intestine. Resveratrol significantly decreases mRNA expression of Lpl, Scd1, Ppar-γ, Acc1, and Fas related to fatty acids synthesis, adipogenesis and lipogenesis, which may be driven by increased Fiaf expression. The Pearson's correlation coefficient shows that there is a negative correlation between the body weight and the ratios of Bacteroidetes-to-Firmicutes. Therefore, resveratrol mediates the composition of gut microbes, and in turn, through the Fiaf signaling pathway, accelerates the development of obesity.

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We investigated the antifungal properties and anti-candidal mechanism of antimicrobial peptide APP. The minimum inhibitory concentration of APP was 8 μM against Candida albicans and Aspeogillus flavus, the concentration against Saccharomyces cerevisiae and Cryptococcus neoformans was 16 μM, while 32 μM inhibited Aspergilla niger and Trichopyton rubrum. APP caused slight depolarization (12.32 ± 0.87%) of the membrane potential of intact C. albicans cells when it exerted its anti-candidal activity and only caused 21.52 ± 0.48% C. albicans cell membrane damage. APP interacted with cell wall membrane, caused potassium efflux and nucleotide leakage. However, confocal fluorescence microscopy experiment and flow cytometry confirmed that FITC-labeled APP penetrated C. albicans cell membrane with 52.31 ± 1.88% cell-penetrating efficiency and accumulated in the cytoplasm. Then, APP interact with C. albicans genomic DNA and completely suppressed DNA migration above weight ratio (peptide/DNA) of 2, and significantly arrested cell cycles during the S-phase (S-phase cell population was 27.09 ± 0.73%, p < 0.05) after penetrating the cell membrane. Results indicated that APP kills C. albicans for efficient cell-penetrating efficiency, strong DNA-binding affinity and significant physiological changes inducing S-phase arrest in intracellular environment.

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Myricetin is an effective antioxidant in the treatment of obesity and obesity-related metabolic disorders. The objective of this study was to explore the regressive effect of myricetin on pre-existing hepatic steatosis induced by high-fat diet (HFD). C57BL/6 mice were fed either a standard diet or a HFD for 12 weeks and then half of the mice were treated with myricetin (0.12% in the diet, w/w) while on their respective diets for further 12 weeks. Myricetin treatment significantly alleviated HFD-induced steatosis, decreased hepatic lipid accumulation and thiobarbituric acid reactive substance (TBARS) levels, and increased antioxidative enzyme activities, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Microarray analysis of hepatic gene expression profiles showed that myricetin significantly altered the expression profiles of 177 genes which were involved in 12 biological pathways, including the peroxisome proliferator activated receptor (PPAR) signaling pathway and peroxisome. Further research indicated that myricetin elevated hepatic nuclear Nrf2 translocation, increased the protein expression of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1), reduced the protein expression of PPARγ, and normalized the expressions of genes that were involved in peroxisome and the PPAR signaling pathway. Our data indicated that myricetin might represent an effective therapeutic agent to treat HFD-induced hepatic steatosis via activating the Nrf2 pathway and the PPAR signaling pathway.

Background China has the largest number of patients with type 2 diabetes mellitus (T2DM) in the world. However, owing to insufficient knowledge of self-management in patients with diabetes, blood glucose (BG) control is poor. Most diabetes-related self-management applications fail to bring significant benefits to patients with T2DM because of the low use rate and difficult operation. Objective This study aims to examine the effectiveness of the combination of the self-designed web-based T2DM management software TangPlan and WeChat on fasting BG (FBG), glycated hemoglobin (HbA1c), body weight, blood pressure (BP), and lipid profiles in patients with T2DM over a 6-month period. Methods Participants were recruited and randomized into the TangPlan and WeChat or control groups. Participants in the control group received usual care, whereas the TangPlan and WeChat participants received self-management guidance with the help of TangPlan and WeChat from health care professionals, including BG self-monitoring; healthy eating; active physical exercise; increasing medication compliance; and health education during follow-ups, lectures, or web-based communication. They were also asked to record and send self-management data to the health care professionals via WeChat to obtain timely and effective guidance on diabetes self-management. Results In this study, 76.9% (120/156) of participants completed the 6-month follow-up visit. After the intervention, FBG (mean 6.51, SD 1.66 mmol/L; P=.048), HbA1c (mean 6.87%, SD 1.11%; P<.001), body weight (mean 66.50, SD 9.51 kg; P=.006), systolic BP (mean 127.03, SD 8.00 mm Hg; P=.005), diastolic BP (mean 75.25, SD 5.88 mm Hg; P=.03), serum low-density lipoprotein cholesterol (mean 2.50, SD 0.61 mmol/L; P=.006), and total cholesterol (mean 4.01, SD 0.83 mmol/L; P=.02) in the TangPlan and WeChat group were all significantly lower, whereas serum high-density lipoprotein cholesterol (mean 1.20, SD 0.25 mmol/L; P=.01) was remarkably higher than in those in the control group. Compared with the baseline data, significance was found in the mean change in FBG (95% CI −0.83 to −0.20; P=.002), HbA1c (95% CI −1.92 to −1.28; P<.001), body weight (95% CI −3.13 to −1.68; P<.001), BMI (95% CI −1.10 to −0.60; P<.001), systolic BP (95% CI −7.37 to −3.94; P<.001), diastolic BP (95% CI −4.52 to −2.33; P<.001), triglycerides (95% CI −0.16 to −0.03; P=.004), serum low-density lipoprotein cholesterol (95% CI −0.54 to −0.30; P<.001), and total cholesterol (95% CI −0.60 to −0.34; P<.001) in the TangPlan and WeChat group but not in the control group (P=.08-.88). Conclusions Compared with usual care for patients with T2DM, the combination of TangPlan and WeChat was effective in improving glycemic control (decrease in HbA1c and BG levels) and serum lipid profiles as well as reducing body weight in patients with T2DM after 6 months. Trial Registration Chinese Clinical Trial Registry ChiCTR2000028843; https://tinyurl.com/559kuve6