Growing evidence highlights the crucial role of gut microbiota in affecting different aspects of obesity. Potential mechanisms for microbial control over eating behavior include microbiota influence on reward and satiety pathways, neurotransmitters release, and hypothalamic-pituitary-adrenal (HPA) axis modulation. A methodology proved to be effective in modulating orexigenic/anorexigenic pathways and food-reward system in obesity is the dTMS. Considering its assets, we hypothesized a potential role of dTMS in inducing weight loss in obesity also via microbiota composition modulation. Twenty-two obese subjects (5 M, 17 F; 44.6±2.5 years; BMI 37.5±1.1 kg/m2) were allocated into 3 groups receiving 15 sessions (3 per week for 5 weeks) of high frequency (18 Hz, HF), low frequency (1 Hz, LF) dTMS, or sham stimulation. Fecal samples were collected at baseline and after 5 weeks of treatment. Total bacterial DNA was extracted from fecal samples using the QIAamp DNA Stool Mini Kit (Qiagen, Italy) and analyzed by a metagenomics approach (Ion Personal Genome Machine). After 5 weeks, a weight loss in HF (-3.4±1.0%; p<0.05) was found, associated with a decrease in norepinephrine (-61.5±15.2%; p<0.01). Furthermore, an increase of Faecalibacterium (+153.3% vs. baseline, p<0.05) and Alistipes (+153.4% vs. baseline, p<0.05) genera, and a significant decrease of Lactobacillus (-77.1% vs. baseline, p<0.05) were found in HF. A significant inverse correlation between Phascolarctobacterium variation and BMI reduction (R:-0.728; p<0.05) was found in HF; norepinephrine change significantly correlated with Eubacterium (R:0.857; p<0.05), Parasutterella (R:0.786; p<0.05), and Streptococcus (R:-0.937; p<0.01) variations.
In conclusion, the weight loss, induced by HF dTMS, improves sympathetic activity and gut microbiota composition in obese subjects, mainly promoting bacterial species with anti-inflammatory properties, that are typical of healthy subjects intestinal flora.
A. Ferrulli: None. M. Toscano: None. M. Adamo: None. I. Terruzzi: None. L. Drago: None. L. Luzi: Speaker's Bureau; Self; A. Menarini Diagnostics, AstraZeneca, Eli Lilly and Company. Research Support; Self; Gelesis. Consultant; Self; McKinsey & Company. Speaker's Bureau; Self; Menarini Group, Merck Sharp & Dohme Corp.. Research Support; Self; Novartis AG. Speaker's Bureau; Self; Novo Nordisk A/S. Research Support; Self; Sunstar Foundation. Speaker's Bureau; Self; Smith & Nephew.