Summary Background An impaired gut microbiota has been reported as an important factor in the pathogenesis of obesity. Weight reduction has already been mentioned to improve gut microbial subpopulations involved in inflammatory processes, though other subpopulations still need further investigation. Thus, weight reduction in the context of a fasting program together with a probiotic intervention may improve the abundance and diversity of gut microbiota. Methods In this pilot study, overweight people underwent a fasting program with laxative treatment for 1 week followed by a 6 week intervention with a probiotic formula. Gut microbiota were analyzed on the basis of 16s rDNA with a quantitative real time polymerase chain reaction. Additionally, a food frequency questionnaire with questions about nutritional behavior, lifestyle, and physical activity was administered before and after the intervention. Results We observed an increase in microbial diversity over the study period. No significant changes in abundance of total bacteria, or of Bacteroidetes, Prevotella, Clostridium cluster XIVa, or Clostridium cluster IV were found, although Faecalibacterium prausnitzii showed an increase over the study period. In addition, Akkermanisa and Bifidobacteria increased in abundance due to intervention. The inflammation-associated gut microbes Enterobacteria and Lactobacilli increased during the first week and then declined by the end of the intervention. Two-thirds of the study participants harbored Archaea. No significant improvements of eating habits were reported, although physical activity improved due to the intervention. Conclusions Our results show that caloric restriction affects gut microbiota by proliferating mucin-degrading microbial subpopulations. An additional intervention with a probiotic formula increased probiotic-administered gut microbial populations.

Obesity is associated with low-grade inflammation, increased ROS production and DNA damage. Supplementation with antioxidants might ameliorate DNA damage and support epigenetic regulation of DNA repair. C57BL/6J male mice were fed a high-fat (HFD) or a control diet (CD) with and without vitamin E supplementation (4.5 mg/kg body weight (b.w.)) for four months. DNA damage, DNA promoter methylation and gene expression of Dnmt1 and a DNA repair gene (MLH1) were assayed in liver and colon. The HFD resulted in organ specific changes in DNA damage, the epigenetically important Dnmt1 gene, and the DNA repair gene MLH1. Vitamin E reduced DNA damage and showed organ-specific effects on MLH1 and Dnmt1 gene expression and methylation. These results suggest that interventions with antioxidants and epigenetic active food ingredients should be developed as an effective prevention for obesity—and oxidative stress—induced health risks.