Background: Adiponectin and resistin are typically secreted by the adipose tissue and are abnormally expressed in obesity. However, the underlying influential factors and mechanisms are to be elucidated. It is well known that the expression of genes is regulated by epigenetics while gut microbiota participates in epigenetic processes through its metabolites such as folate, biotin, and short-chain fatty acids (SCFAs). Therefore, we supposed that alteration of gut microbiota might affect the transcriptional expression of adiponectin and resistin through epigenetic regulation in obesity. Methods: C57BL/6J mice were fed either a high-fat diet (34.9% fat by wt., 60% kcal) or a normal-fat diet (4.3% fat by wt., 10% kcal) for 16 weeks, with ampicillin and neomycin delivered via drinking water to interfere with gut microbiota development. Fecal microbiota was analyzed by 16S rRNA high-throughput sequencing. The mRNA expression levels of genes were measured by real-time quantitative RT-PCR. SCFA contents in feces were examined using gas chromatography. Results: Alteration of the gut microbiota induced by antibiotic use, characterized by a dramatic reduction of the phylum Firmicutes and Actinobacteria and an increase of Proteobacteria with reductions of genera including Lactobacillus, norank_f_Bacteroidales_S24-7_group, Alistipes, Desulfovibrio, Helicobacter, etc., and increases in Bacteroides, Enterobacter, Klebsiella, inhibited the body weight gain in mice fed the high-fat diet instead of the normal-fat diet. The mRNA expression of adiponectin and resistin was upregulated by antibiotic use in mice fed the high-fat diet, accompanied by increased expression of fat oxidation and thermogenesis-related genes (PPAR-α, Pgc-1α, and Atgl) in the fat and/or liver, whereas no change in the expression of adiponectin and resistin was found in mice fed the normal-fat diet. Furthermore, antibiotic use reduced DNA methylation fractions of the adiponectin and resistin promoters and downregulated the expression of DNA methyltransferase 1 and 3a (DNMT1 and DNMT3a) with the high-fat diet feeding. Conclusion: Alteration of gut microbiota induced by antibiotic use may affect the expression of adiponectin and resistin in mice fed the high-fat diet by modifying promoter DNA methylation, thus leading to increased fatty acid oxidation and less body weight gain.

Vinegar is widely used in Chinese diet as a traditional condiment, and its functional component acetic acid has been proposed to prevent obesity, while its mechanism is still unclear. Bile acids (BAs) have been reported to have a protective effect on obesity. This study demonstrated that high-fat diet induced obesity (DIO) seriously disturbed BAs balance by significantly decreasing hepatic BAs synthesis and increasing fecal BAs excretion. However, acetate supplemented in the high-fat diet can restore BAs balance by mainly promoting hepatic taurine conjugated BAs (tauro-BAs) synthesis and decreasing fecal tauro-BAs excretion. The tauro-BAs, as the antagonists, inhibited the intestinal-liver farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15)-FGF receptor 4 (FGFR4) signaling pathway, and negatively regulated the production of hepatic BAs. Present study provided important clues for further investigation of the mechanism of acetic acid inhibiting DIO.

Background: Telomeres play a crucial role in cellular survival and its length is a predictor for onset of chronic non-communicable diseases. Studies on association between telomeres and obesity in children have brought discrepant results and the underlying mechanisms and influential factors are to be elucidated. This study aimed to investigate changes in telomere length and telomerase reverse transcriptase (TERT) DNA methylation, and further to determine their correlation with n-3 polyunsaturated fatty acids (PUFAs) in preschool children with obesity. Methods: Forty-six preschool children with obesity aged 3 to 4 years were included in the study, with equal numbers of age- and gender-matched children with normal weight as control. Leukocyte telomere length was determined by the ratio of telomeric product and single copy gene obtained using real-time qPCR. DNA methylation of TERT promoter was analyzed by bisulfite sequencing. Fatty acids in erythrocytes were measured by gas chromatography with a total of 15 fatty acids analyzed. The total saturated fatty acids (SFAs), total n-6 PUFAs, total n-3 PUFAs, and the ratio of arachidonic acid (AA) to docosahexaenoic acid (DHA) were calculated. Then the correlation between leukocyte telomere length, TERT promoter methylation and fatty acids was determined. Results: In preschool children with obesity, leukocyte telomeres were shortened and had a negative association with the body mass index. The methylated fractions in 13 of 25 CpG sites in the TERT promoter were increased by approximately 3 to 35% in the children with obesity compared to the normal weight children. Erythrocyte lauric acid and total SFAs, lenoleic acid and total n-6 PUFAs were higher, and DHA was lower in the children with obesity than those in the children with normal weight. Correlative analysis showed that leukocyte telomere length had a positive association with total SFAs and DHA, and a negative association with the AA/DHA ratio. However, no association between erythrocyte DHA and the TERT promoter methylation was found. Conclusion: These data indicate that the reduced body DHA content and increased AA/DHA ratio may be associated with shortened leukocyte telomeres in child obesity, which is probably not involved in the TERT promoter methylation.

Antibiotic resistance genes (ARGs) threaten the success of modern drugs against multidrug resistant infections. ARGs can be transferred to opportunistic pathogens by horizontal gene transfer (HGT). Many studies have investigated the characteristics of ARGs in various chemical stressors. Studies on the effects of dietary nutrition and dietary patterns on ARGs are rare. The study first demonstrated the effect of calorie restricted (CR) diet on the ARGs and mobile genetic elements (MGEs) in mouse feces and explored their relationship with gut microbiota and their functions. The results showed that the abundance of the total ARGs in mouse feces of the CR group increased, especially tetracycline ARGs (tetW-01). The abundance of the MLSB ARGs (ermB) decreased evidently in mouse feces of the CR group. In addition, the total abundance of MGEs decreased evidently in the CR group, especially tnpA-03. In the meantime, the abundance of Lactobacillus and Bifidobacterium in mouse feces of the CR group increased remarkably. The Spearman correlation analysis between gut microbiota and ARGs showed that several probiotics were significantly positively correlated with ARGs (tetW-01), which might be the main contribution to the increase in ARGs of the CR group.