Sleeve Gastrectomy and Roux-en-Y Gastric Bypass Alter the Gut-Brain Communication

Ballsmider, L. A.; Vaughn, Alexandra C; David, Matan Ben; Hajnal, A.; Lorenzo, Patricia M. Di; Czaja, Krzysztof

doi:10.1155/2015/601985

Cited by 63 publications

(52 citation statements)

References 63 publications

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“…Similar to vagotomy, it is possible that inflammation-mediated damage to the gastric vagus system may reduce food intake and increase satiety signaling in these animals [62, 63]. Consumption of HF, highly palatable food in rodents has been shown to promote hyperphagia.…”

Section: Resultsmentioning

confidence: 99%

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Sen

Cawthon

Ihde

et al. 2017

Physiology & Behavior

203

152

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Obesity is one of the major health issues in the United States. Consumption of diets rich in energy, notably from fats and sugars (high-fat/high-sugar diet: HF/HSD) is linked to the development of obesity and a popular dietary approach for weight loss is to reduce fat intake. Obesity research traditionally uses low and high fat diets and there has been limited investigation of the potential detrimental effects of a low-fat/high-sugar diet (LF/HSD) on body fat accumulation and health. Therefore, in the present study, we investigated the effects of HF/HSD and LF/HSD on microbiota composition, gut inflammation, gut-brain vagal communication and body fat accumulation. Specifically, we tested the hypothesis that LF/HSD changes the gut microbiota, induces gut inflammation and alters vagal gut-brain communication, associated with increased body fat accumulation. Sprague-Dawley rats were fed an HF/HSD, LF/HSD or control low-fat/low-sugar diet (LF/LSD) for 4 weeks. Body weight, caloric intake, and body composition were monitored daily and fecal samples were collected at baseline, 1, 6 and 27 days after the dietary switch. After four weeks, blood and tissues (gut, brain, liver and nodose ganglia) were sampled. Both HF/HSD and LF/HSD-fed rats displayed significant increases in body weight and body fat compared to LF/LSD-fed rats. 16S rRNA sequencing showed that both HF/HSD and LF/HSD-fed animals exhibited gut microbiota dysbiosis characterized by an overall decrease in bacterial diversity and an increase in Firmicutes/Bacteriodetes ratio. Dysbiosis was typified by a bloom in Clostridia and Bacilli and a marked decrease in Lactobacillus spp. LF/HSD-fed animals showed a specific increase in Sutterella and Bilophila, both Proteobacteria, abundances of which have been associated with liver damage. Expression of pro-inflammatory cytokines, such as IL-6, IL-1β and TNFα was upregulated in the cecum while levels of tight junction protein occludin were downregulated in both HF/HSD and LF/HSD fed rats. HF/HSD and LF/HSD-fed rats also exhibited an increase in cecum and serum levels of lipopolysaccharide (LPS), a pro-inflammatory bacterial product. Immunofluorescence revealed the withdrawal of vagal afferents from the gut and at their site of termination the nucleus of the solitary tract (NTS) in both the HF/HSD and LF/HSD rats. Moreover, there was significant microglia activation in the nodose ganglia, which contain the vagal afferent neuron cell bodies, of HF/HSD and LF/HSD rats. Taken together, these data indicate that, similar to HF/HSD, consumption of an LF/HSD induces dysbiosis of gut microbiota, increases gut inflammation and alters vagal gut-brain communication. These changes are associated with an increase in body fat accumulation.

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Section: Resultsmentioning

confidence: 99%

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Sen

Cawthon

Ihde

et al. 2017

Physiology & Behavior

203

152

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“…The increase in the density may reflect a sprouting of vagal inputs into the hindbrain feeding centers. Interestingly, our previous studies revealed that damage to peripheral axons of the vagus (subdiaphragmatic vagotomy) also induced transient decrease in the density of vagal afferents projecting to the NTS (Ballsmider et al 2015, Peters et al 2013) followed by vagal inputs sprouting. Vagal damage also resulted in microglia activation in the NTS and DMV (Gallaher et al 2012).…”

Section: Discussionmentioning

confidence: 98%

Energy‑dense diet triggers changes in gut microbiota, reorganization of gut‑brain vagal communication and increases body fat accumulation

Vaughn¹,

Cooper²,

Lorenzo³

et al. 2017

Acta Neurobiologiae Experimentalis

130

105

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Obesity is associated with consumption of energy-dense diets and development of systemic inflammation. Gut microbiota play a role in energy harvest and inflammation and can influence the change from lean to obese phenotypes. The nucleus of the solitary tract (NTS) is a brain target for gastrointestinal signals modulating satiety and alterations in gut-brain vagal pathway may promote overeating and obesity. Therefore, we tested the hypothesis that high-fat diet-induced changes in gut microbiota alter vagal gut-brain communication associated with increased body fat accumulation. Sprague-Dawley rats consumed a low energy-dense rodent diet (LFD; 3.1 kcal/g) or high energy-dense diet (HFD, 5.24 kcal/g). Minocycline was used to manipulate gut microbiota composition. 16S Sequencing was used to determine microbiota composition. Immunofluorescence against IB4 and Iba1 was used to determine NTS reorganization and microglia activation. Nodose ganglia from LFD rats were isolated and co-cultured with different bacteria strains to determine neurotoxicity. HFD altered gut microbiota with increases in Firmicutes/Bacteriodetes ratio and in pro-inflammatory Proteobacteria proliferation. HFD triggered reorganization of vagal afferents and microglia activation in the NTS, associated with weight gain. Minocycline-treated HFD rats exhibited microbiota profile comparable to LFD animals. Minocycline suppressed HFD-induced reorganization of vagal afferents and microglia activation in the NTS, and reduced body fat accumulation. Proteobacteria isolated from cecum of HFD rats were toxic to vagal afferent neurons in culture. Our findings show that diet-induced shift in gut microbiome may disrupt vagal gut-brain communication resulting in microglia activation and increased body fat accumulation.

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“…Recent rodent studies indicate that major neuronal reorganization takes place in lower brainstem after bariatric interventions (Ballsmider et al, 2015). Future research may reveal novel pathways linking brainstem function to duodenal-sensitive dopamine cells.…”

Section: Discussionmentioning

confidence: 99%

Striatal Dopamine Links Gastrointestinal Rerouting to Altered Sweet Appetite

et al. 2016

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Reductions in calorie intake contribute significantly to the positive outcome of bariatric surgeries. However, the physiological mechanisms linking the rerouting of the gastrointestinal tract to reductions in sugar cravings remain uncertain. We show that a duodenal-jejunal bypass (DJB) intervention inhibits maladaptive sweet appetite by acting on dopamine-responsive striatal circuitries. DJB disrupted the ability of recurrent sugar exposure to promote sweet appetite in sated animals, thereby revealing a link between recurrent duodenal sugar influx and maladaptive sweet intake. Unlike ingestion of a low-calorie sweetener, ingestion of sugar was associated with significant dopamine effluxes in dorsal striatum, with glucose infusions into the duodenum inducing greater striatal dopamine release than equivalent jejunal infusions. Consistently, optogenetic activation of dopamine-excitable cells of dorsal striatum was sufficient to restore maladaptive sweet appetite in sated DJB mice. Our findings point to a causal link between striatal dopamine signaling and the outcomes of bariatric interventions.

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Sleeve Gastrectomy and Roux-en-Y Gastric Bypass Alter the Gut-Brain Communication

Cited by 63 publications

References 63 publications

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Energy‑dense diet triggers changes in gut microbiota, reorganization of gut‑brain vagal communication and increases body fat accumulation

Striatal Dopamine Links Gastrointestinal Rerouting to Altered Sweet Appetite

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