**4. Effects of bariatric surgery methods on gut microbiota**

#### **4.1 Roux-en-Y gastric bypass (RYGB)-gut microbiota**

Bariatric surgery modifies the gut microbiota. Bariatric surgery also affects the physiology of the distal intestine and has a great influence on activity and the

#### *Do All Bariatric Surgery Methods Have the Same Effects on the Gut Microbiota? DOI: http://dx.doi.org/10.5772/intechopen.107176*

composition of the gut microbiota. Different methods of bariatric surgery alter the intestinal microbiota differently [39]. Bacterial diversity and richness are restored by RYGB surgery, and the frequency of several groups of bacteria is significantly altered [40]. These changes after surgery may affect weight loss, weight maintenance, and metabolic improvement. They may also cause weight gain [40, 41]. Patients who lost weight successfully after RYGB surgery had a significant difference in gut microbiota compared to patients who showed weight regain [41]. Patient preferences for high-fat and high-carbohydrate foods decrease after RYGB surgery. Patients have reportedly lost motivation to eat. Another common effect of RYGB surgery is to alter the gut microbiota and its related metabolites. *Escherichia Coli, Streptococcus, pneumonia, Klebsiella, Akkermansia muciniphila*, *Dentium*, and *Bifidobacterium* in the feces of patients increased after RYGB surgery [42]. After RYGB surgery, there is a decrease in *Firmicutes* and an increase in the frequency of *Verrucomicrobia* (*Akkermansia*) and *proteobacteria* in patients. After surgery, the *phylum Bacteroidetes* abundance decreases. Also, there is a decrease in the genus *Clostridium* and abundance of *the Fusobacteriaceae* family. *Gammaproteobacteria* (including *Enterobacteriaceae*), and the genus *Succinivibrio* increased following RYGB. Also, after surgery in animals and humans, an increase in *Enterococcus* was observed. This genus competes for intestinal epithelium adherence, and hereby, prevents the colonization of pathogenic bacteria and also has anti-inflammatory effects by producing butyrate [41]. After RYGB, the pH of the intestinal is lower compared to SG. Excluded parts of digestive transit in RYGB are the distal stomach and small intestine. Therefore, avoided stomach acidity and in the intestine, hydrochloric acid is reduced. Some studies have shown the pH reduction effect in inhibiting *Bacteroidetes* growth in bacterial culture. pH is important in the distribution of fermentation end-products [39]. After RYGB, a decrease in gastric acid secretion causes the incompletely digested proteins to increment in the gut and this results in the production of putrescine. Bacteria of the genus *Klebsiella* that has increased after RYGB. Also, can produce putrescine. This polyamine is metabolized to GABA, which stimulates the GLP-1 levels increments and improves insulin resistance. Similarly, the genus *Lachnobacterium,* which increased after RYGB improves glucose homeostasis and insulin resistance via short-chain fatty acids [41]. Metabolites like short-chain fatty acids produced by the intestinal microbiota have a beneficial effect on health and they have been linked to glycemic improvement, food intake regulation, and weight loss [43]. When the obese diabetic patients' fecal microbiota is evaluated before and after RYGB surgery, and preoperatively increase in *desulfovibrio* levels is seen in patients who have no postoperative T2DM remission compared with patients who have metabolic improvement [44]. Species, such as *pneumonia, Klebsiella, Alistipes, muciniphila*, and *Akkermansia,* are species that are augmented after RYGB and their relative abundance is associated with reduced adiposity [45]. There is *Streptococcus* and *villanelle* increment and *Claudia decrement* (all belong to the *Firmicutes phylum*). These changes can have important clinical consequences after surgery. For example, *Streptococcus* and *Veillonella* metabolize lactate, which in turn affects butyrate metabolism and epithelial barrier integrity. Increasing the integrity of the intestinal epithelium can improve metabolic disorders and reduce low-grade systemic inflammation. *Akkermensia* contains mucin-destroying microbes and in several studies has been shown increment after bariatric surgery. According to previous animal studies, *Akkermensia muciniphila* has been shown to protect against diabetes and obesity by potentially reducing low-grade inflammation and endotoxemia, as well as enhancing the barrier of the intestinal epithelium. *Akkermensia muciniphila* in humans also was associated with improved insulin sensitivity markers. A negative correlation has previously been reported between serum leptin and *E. Coli* after RYGB [43]. Reducing stomach volume, which is included in RYGB, dramatically reduces the amount of food intake. Individual changes in diet can alter gut microbiota and it should be considered when considering changes in gut microbiota after bariatric surgery procedures [44]. Hospital-associated pathogens, such as *pneumonia, Klebsiella*, and *clostridium,* perfringens have also been shown to increase after RYGB. After surgery, one of the reasons for opportunistic pathogens increments is the routine administration of operative prophylactic antibiotics and alternation of the gastrointestinal environment [43]. RYGB surgery procedure resulted in a significant reduction in estimated and observed fungal diversity and richness. This contradicts many reports of bacterial alpha diversity increments. Despite the unidirectional changes observed in bacterial microbiota, changes in fungal microbiota after RYGB are individual [40].

#### **4.2 Laparoscopic sleeve gastrectomy (LSG)-gut microbiota**

Changes in the composition of the gut microbial community after surgery can affect metabolic outcomes. In particular, SG alters certain gut bacteria's relative abundance. It leads to increases in the species that improve the phenotypes of diabetes and obesity, abundance. For obese mice, fecal transplantation from mice and human patients post-bariatric surgery has metabolic benefits, such as improved insulin sensitivity, glucose tolerance, and weight loss. Importantly, in mice, antibiotics abolish the SG effectiveness due to gut microbiota disruption. These findings increase the possibility that after SG in metabolic changes gut bacteria are involved. Gut bacteria communicate through the portal vein by transporting a bacterial-derived molecule from the intestine to the liver [46]. SG leads to persistent changes in the intestinal microbiome by decreasing dysbiosis due to an increase in *Bacteroidetes* and a decrease in *Firmicutes*. SG improves diurnal oscillation and dysbiosis and increases microbial richness [47]. Compared to before LSG the percentage of *Phylum Verrucomicrobia* significantly increased after 1 month and 6 months. Percentages for the *Streptococcaceae* family also significantly increased. Also, *Christensenellaceae* increased after 1 month and 3 months, *Verrucomicrobiaceae* increased after 1 month and 6 months, *Rikenellaceae* increased after 6 months, and *Fusobacteriaceae* increased after 2 weeks, *A. muciniphila* significantly increased after 1 month and 6 months. For gut microbiota, the diversity indices OS, PD, and Chao1 were significantly increased after 6 months. The percentage of *Mogibacteriaceae* family after 3 months and 6 months were significantly decreased than before LSG [48]. SG surgery does not affect the presence of *F. Prausnitzii*, a butyrate producer in feces. LRYGB resulted in a greater increase in oral colonizers (genus *Veillonela* and *Streptococcus*) than in SG. *A. Muciniphila*, which negatively correlated with inflammation, increases in a similar proportion in patients after LRYGB or SG. *E. Coli* increment may reflect gut and host adaptation to energy harvest maximization in the post-bariatric surgery starvation-like condition [49]. In a rodent model, it was shown that *A. Muciniphila* inhibited metabolic abnormalities and body fat accumulation. However, with decreasing biological parameters related to obesity, increasing diversity of α and other taxa like *the Rikenellaceae* family is more associated. Although not much attention has been paid to *Rikenellaceae*, the results suggest that *the Rikenellaceae* taxon may play a role in the metabolic benefits of LSG and weight loss [48]. Changes in the microbiome after SG, particularly the reduction of *Clostridia*, lead to a decrease in lithocholic acid (LCA) production, which ultimately

#### *Do All Bariatric Surgery Methods Have the Same Effects on the Gut Microbiota? DOI: http://dx.doi.org/10.5772/intechopen.107176*

leads to increased glucoregulatory compound CA7S production. Lithocolicacid (LCA) by inducing CA7S synthesis in murine liver and human hepatocytes affects host metabolism. After SG, the amount of lithocholic acid (LCA) that is transported from the intestine to the liver through the portal vein increases. LCA induces colonic acid sulfonation and activates vitamin D receptors both *in vivo* in mice and *in vitro* in human hepatocytes. CA7S synthesized by LCA in human hepatocytes can induce the secretion of GLP-1 in enteroendocrine cells and provides a link between the changes in BA observed after SG and the surgery's metabolic benefits [46]. After LSG, *Fusobacteriaceae* and *Streptococcaceae* families relative abundance increased. These species are thought to have a pathogenic property, such as colorectal carcinogenic risk. They may be high due to reduced gastric passage time and decreased gastric juice secretion by LSG. After LSG, although the α diversity index is restored, the total number of gut microbiota remains lower than in healthy individuals. Disorders, such as Parkinson's disease, colorectal cancer, and inflammatory bowel disease, are associated with decreased total microbiota [48]. *Pseudobutyrivibrio* and *Prevotella sp.* increase after SG, they can inhibit colon cancer cell formation [50]. *Clostridium* species became enriched after SG, while LRYGB harmed them, which suggests the intestine is still largely anaerobic after SG. In this regard, a higher ferredoxin oxidoreductase relative abundance was observed post-LRYGB compared to SG, which is associated generally with aerobic respiration [49]. After SG Microbiome changes may protect from progressive hypertension related to multiple strains of *Lactobacillus* [51]. After 9 years postoperatively, changes in gut microbiota are less pronounced in LSG patients versus RYGB patients [52].
