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Roux-En-Y Gastric Bypass (RYGB) Surgery
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This entry is adapted from the peer-reviewed paper 10.3390/ijms23031126

Roux-en-Y gastric bypass (RYGB) surgery has been proven successful in weight loss and improvement of co-morbidities associated with obesity. Chronic complications such as malabsorption of micronutrients in up to 50% of patients underline the need for additional therapeutic approaches. 

RYGB metabolomics microbiome

1. Introduction

Roux-en-Y gastric bypass (RYGB) surgery is the most frequently employed bariatric technique in Western countries [1]. The surgical intervention consists of transection of the stomach, leaving a small gastric pouch, which is anastomosed to a distal part of the small intestine, creating a Roux (dietary) limb [2]. The rearrangement of the gut allows ingested food direct access to the small intestinal lumen, where it is eventually joined with the biliopancreatic limb, from which point the common channel is formed. After RYGB surgery, patient preferences for high-carbohydrate and high-fat foods decreased [3][4], and patients reportedly lost the motivation to eat [3]. Similarly, the preference for a high-fat diet steadily decreased, and the preference for a standard low-fat chow increased over a five-month post-surgical period in a rat model of RYGB [5].
RYGB surgery improves metabolic health and diabetes remission more effectively than other treatment strategies, including pharmacotherapy and lifestyle interventions [6][7]. Several murine RYGB studies show a positive impact of the surgery on various metabolic parameters reducing the risk of type 2 diabetes mellitus [8][9][10] and hyperlipidemia [11]. RYGB surgery leads to reduced glycemia, as shown by functional studies of the liver and brain. Surgery led to an improvement in liver health and glycemic control, further reducing the risk of hepatic steatosis [12]. RYGB surgery was also reported to lower lipogenesis and increase fatty acid beta-oxidation in the type 2 diabetes rat model [12]. Moreover, indications of lowered glycemia were also reported by a positron emission tomography (PET) imaging study where increased neuronal activity was shown in the hypothalamic and thalamic brain regions [13].

2. Liquid Sucrose-Induced Obesity Is Reverted by RYGB Surgery

The persistent weight reduction in liquid sucrose diet-induced obese rats post-RYGB surgery, similar to other animal studies [1][14] and clinical practice [15]. PF animals had similar body weight to the AdLib group after the sham surgery, suggesting that caloric restriction was not the only driver for the RYGB-induced weight loss. Moreover, caloric restriction efficiently reduced total liver fat content in the PF animals. While the total energy consumption was significantly higher in AdLib compared to RYGB and therefore also PF, the relative percentage of energy consumed via liquid sucrose was not significantly changed between the groups. The surgery led to a reduced total energy intake in RYGB animals.

3. Microbiota Perturbations Lead to Upregulated Fecal GABA and Lower Fiber Fermentation

RYGB surgery causes a persistent environmental change of the gut which has been previously associated with a long-lasting impact on the microbiota composition and metabolism [16]. RYGB has also been shown to promote a change in dietary habits and their associated neuronal processes [17]. Bacteroidetes and Proteobacteria such as Escherichia have been reported to actively express the genes necessary for producing the neurotransmitter GABA in human stool [18]. GABA is a crucial part of the brain’s GABAergic system and the enteric nervous system (ENS), acting as a modulator for the gut signaling processes [19]. It has been reported that GABA can activate gut/intestinal cells and further promote a cascade leading to neuronal cell activation via gut secreted exosomes [20]. GABA receptors also have been shown to influence the liquid secretion processes (GABA-A) and gut motility (GABA-B) [21]. Increased GABA concentrations in feces correlate to the liquid state of the feces and suggest a higher defecation rate in RYGB compared to sham groups.
Lower levels of fecal SCFA in RYGB and AdLib compared to PF may result from different nutrient availability in the colon. In RYGB, this is a potential side effect of surgery and consequent malabsorption as the macronutrients can escape directly from the small intestine into the large intestine. While in AdLib, similarly lower SCFA was quantified due to the larger amount of food ingested, and thus more macronutrients entered the fermentative section of the gut. As the substrate is different, the readily available macronutrients such as protein and simple carbohydrates might be fermented first and fast by the microbiota, giving the SCFA more time for entering enterocytes and the bloodstream via diffusion, resulting in lower fiber fermentation and therefore less SCFA in RYGB and AdLib feces compared to PF.
Moreover, the higher relative abundance of Bacteroidetes, particularly Muribaculaceae species, which are versatile carbohydrate degraders [22], could indicate a shift from fiber fermentation to host-derived carbohydrate utilization in the microbiome of RYGB animals [23][24].
Increased fecal taurine in RYGB has been previously reported in the context of the intestinal NOD-like receptor family pyrin domain containing 6 (NLRP6) inflammasome expression repair leading to gut immune homeostasis [25] and supports our findings of reduced inflammation in RYGB as reflected by decreased CRP plasma levels.
TMA and TMAO were elevated in the feces of RYGB rats and are usually produced from dietary choline and carnitine by gut bacterial enzymes (choline TMA lyase; carnitine oxidoreductase) [26][27]. In our dataset, plasma TMA and TMAO had a significant positive correlation to the relative abundance of Enterococcus, most prominent at four and eight weeks post-surgery. Enterococcus species have been reported to enable plasma TMAO degradation ex vivo [28], suggesting that bacterial species could be activated with the purpose of TMA and TMAO degradation. TMA and TMAO have been related to increased risk of cardiovascular disease [29][30][31]. 

4. RYGB Surgery Leads to Lowered Plasma BCAA and Increased Glycine

Plasma metabolite profiling confirmed that RYGB surgery alters the valine, leucine, and isoleucine BCAA biosynthesis pathway [32]. BCAA upregulation has been linked to obesity and diabetes [33] and interconnected with glycine downregulation [34]. Reduced solid food intake resulted in less available protein in RYGB and PF. However, quantified BCAA decrease could indicate malabsorption in RYGB.
Metabolites such as serine and glycine are known substrates for the folate and methionine cycle [35]. These further participate in one-carbon metabolism, which is crucial for appropriate nucleotide and cofactor synthesis. Obesity and type 2 diabetes have been previously associated with depleted circulating glycine and the potential necessity of therapeutic glycine supplementation [36]. RYGB surgery leads to improved plasma metabolite patterns and, therefore, a potentially reduced risk of type 2 diabetes.

5. RYGB Surgery Results in Elevated LBP Not as a Result of Inflammation but Possibly from Increased Lipolysis as Seen by Plasma Ketone Body Levels

Although increased LBP in plasma is a known marker for inflammation [37], the researchers did not observe any other signs for an upregulated inflammatory response in the RYGB group compared to the sham. Indeed, plasma CRP levels were decreased in RYGB compared to sham groups, which is in good agreement with previous research [38]. Increased hepatic even/odd chain fatty acid ratio and reduced leptin levels in RYGB support the hypothesis that RYGB leads to upregulated lipolysis as reflected by increased levels of the ketone body 3-hydroxybutyrate in RYGB animal plasma. 3-Hydroxybutyrate is produced by the liver in lipolysis and serves as the primary energy substrate via beta-oxidation and acetyl-CoA for the TCA cycle when glucose is depleted [39]. During lipolysis, long-chain fatty acids can be transported only within chylomicrons, which are therefore highly upregulated [40]. However, as LPS has a high affinity for chylomicrons, chylomicron formation due to increased lipolysis promotes intestinal LPS absorption, as previously described in gut mucosa [38]. 
The decrease of the ketogenic amino acid lysine in RYGB feces and increased 3-hydroxybutyrate in RYGB plasma indicates that lysine could be transformed into 3-hydroxybutyrate. It is important to note that increased 3-hydroxybutyrate has also been found in humans after one-anastomosis gastric bypass surgery [41].

6. The Even/Odd Saturated FA Ratio Is Increased after RYGB Surgery

The RYGB hepatic FA profiles differed from the PF and AdLib animals when considering the hepatic even/odd FA ratio, which was higher in RYGB. Indeed, RYGB animals showed a lower concentration of margaric acid (C17:0) than sham animals, which could be synthesized in the liver from the gut-derived propionate, a metabolite found in reduced concentrations in the RYGB feces. It is well recognized that gut microbiota influences host lipid metabolism [42]. Kindt et al. showed that microbiota-derived dietary fiber acetate leads to the synthesis of FA in the liver, particularly palmitic acid (C16:0) and stearic acid (C18:0). Moreover, fructose triggers de novo lipogenesis in the liver through two mechanisms, both involving its transformation into acetate by the microbiota [42]. Moreover, the liver can use gut-derived propionate to synthesize odd chain FA [43].  Kindt et al. showed that changes in FA profiles in the liver were also found in plasma FA profiles and might, therefore, have a systemic effect. It has also been shown that the circulating long-chain FA can be sensed in the hypothalamus, where they regulate glucose homeostasis [44]. Nevertheless, the researchers did not find a direct gut-brain link through our investigation.

7. RYGB Surgery Leads to Altered Neuronal Activity in the Rat Brain

The highest neuronal activation was observed in RYGB compared to sham rats in the brain stem, midbrain, thalamus, and hypothalamus areas. The midbrain regions of ctg and DpMe are GABAergic cell-rich regions with a high potential for GABAergic signaling processes [45]. They are involved in an exaggerated activation of homeostatic feeding circuits and display enhanced brain serotonergic signaling after RYGB surgery [46].
3-HPPA has been reported to be able to cross the blood-brain barrier, further serving as a competitive inhibitor for dopamine synthesis [47]. Although a limitation of this study was the relatively low animal number per group, the RYGB surgery results in increased neuronal activity in the RYGB animals compared to controls.

8. Key Findings and Future Implications

In conclusion, RYGB surgery successfully reversed the weight gain induced by the liquid sucrose diet. In the gut, RYGB rats showed increased Bacteriodota, Probacteria, and decreased Firmicutes. Microbiota changes led to notably increased GABA production in the gut, which further quantified in feces, possibly influencing downstream metabolite and cytokine profiles as well as signaling in GABAergic regions of the ENS and CNS. Lowered plasma BCAA and increased glycine in RYGB suggested a lowered risk of obesity. 

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