Gut microbiome modified by bariatric surgery improves insulin sensitivity and correlates with increased brown fat activity and energy expenditure

Gut microbiota and therapy for obesity and type 2 diabetes

“…Firmicutes were significantly decreased whereas Bacteroidetes were significantly increased in the individuals post-RYGB. Moreover, Akkermansia became prominent in post-gastricbypass individuals, comparable to the individuals with normal body weight (96,117,118). The abundance of F. prausnitzii, which was directly correlated to fasting blood glucose, was lower in individuals with morbid obesity with or without diabetes before RYGB, but increased three months post-RYGB and remained stable until the study end point -six months post-RYGB (97,120).…”

Exploring a novel therapeutic strategy: the interplay between gut microbiota and high-fat diet in the pathogenesis of metabolic disorders

“…By transferring fecal microbiota transplantation to the host or feeding probiotics, obesity phenotype indicators can be improved, and the levels of HDL-C, LDL-C, adiponectin, leptin, and TNF-α can be regulated ( 116 , 119 – 121 ). Animal experiments have also found that obese mice receiving microbiota from post-bariatric surgery mice showed enrichment of mucin-degrading Akkermansia muciniphila or Bacteroides fragilis , increased levels of tryptophan-derived metabolites, SCFAs, and acylcarnitines, increased brown fat mass and activity, increased energy expenditure, and improved immune homeostasis in white adipose tissue ( 122 ). Clinical studies have also observed similar phenomena, and the mechanism behind this may be that the gastric bypass-shaped gut microbiota reactivates the energy expenditure of metabolically active brown adipose tissue through the bile acid receptors FXR-TGR5, thereby reducing obesity in diet-induced obese patients ( 121 ).…”

Gut microbiota turn up the heat after bariatric surgery

“…While both gut microbiota and bariatric surgery have been shown to activate thermogenesis in fat [14], their connection has, until recently, not been addressed. Two new studies by Jin et al [15] and Yadav et al [16] now provide causal evidence, using complementary approaches, that VSG and RYGB activate thermogenesis in fat through distinct microbiota-dependent mechanisms, to in turn promote metabolic health.…”

“…In the other study by Yadav et al [16] stool samples were collected from 4 patients with morbid obesity before and 1-6 months after RYGB, and subsequently transferred to germ-free mice. What sets the approach of Yadav et al [16] apart from similar studies is that samples before and after RYGB from the same individual patient were orally gavaged into recipient germ-free mice in a longitudinal design rather than in a cross-sectional design, which preserves the inter-individual variability in the response to bariatric sugery. Another notable detail of the study of Yadav et al [16] is that the germ-free mice in their study were rendered obese on a sterile and costly Western-style diet prior to receiving stool samples from patients.…”

“…What sets the approach of Yadav et al [16] apart from similar studies is that samples before and after RYGB from the same individual patient were orally gavaged into recipient germ-free mice in a longitudinal design rather than in a cross-sectional design, which preserves the inter-individual variability in the response to bariatric sugery. Another notable detail of the study of Yadav et al [16] is that the germ-free mice in their study were rendered obese on a sterile and costly Western-style diet prior to receiving stool samples from patients. Perhaps equally as important is the delayed timepoint after fecal microbiota transfer (12 weeks) that recipient germ-free mice were subjected to metabolic phenotyping, allowing sufficient time for the transferred fecal microbiota to expand and colonize the gastrointestinal tract and exert metabolic effects.…”