Vagal innervation patterns following Roux-en-Y gastric bypass in the mouse

Division of Hypothalamic Research, Department of Internal Medicine, UT Southwestern Medical Center at Dallas, Dallas, TX, USA.
International journal of obesity (2005) (Impact Factor: 5). 03/2013; 37(12). DOI: 10.1038/ijo.2013.48
Source: PubMed


This study investigated the anatomical integrity of the vagal innervation to the gastrointestinal tract following Roux-en-Y gastric bypass (RYGB) in the mouse. Specifically, the surgical procedure was performed in high-fat-fed reporter mice (Phox2b-Cre-tdTomato), in which the entire vagal innervation of the gastrointestinal tract was fluorescently labeled. As a result, our anatomical observations revealed both qualitative and quantitative changes of the vagal supply to the gut after RYGB. This included the extensive denervation of the glandular and distal stomach, and sites of surgical interventions (clipping and anastomosis). Furthermore, the stomach wall after RYGB frequently contained dystrophic axons and endings, suggestive of vagal neurodegeneration. In contrast, RYGB did not significantly modify the innervation to the rest of the intestines and glucostatic organs. In summary, the present study describes a previously unrecognized pattern of vagal remodeling and denervation following RYGB. Our findings may serve as a guideline for future investigations on the role of gut-brain communication in bariatric surgery.International Journal of Obesity advance online publication, 23 April 2013; doi:10.1038/ijo.2013.48.

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Available from: Laurent Gautron, Aug 29, 2015
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    • "Notably, recent reports indicate that sensitivity of vagal innervation to specific gastrointestinal stimuli is enhanced in obesity [21] [22] and after bariatric intervention [23]. However, much less is known regarding the reorganization of vagal innervation following the bariatric operation [24]. "
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    ABSTRACT: This study investigated the anatomical integrity of vagal innervation of the gastrointestinal tract following vertical sleeve gastrectomy (VSG) and Roux-en-Y gastric bypass (RYGB) operations. The retrograde tracer fast blue (FB) was injected into the stomach to label vagal neurons originating from nodose ganglion (NG) and dorsal motor nucleus of the vagus (DMV). Microglia activation was determined by quantifying changes in the fluorescent staining of hindbrain sections against an ionizing calcium adapter binding molecule 1 (Iba1). Reorganization of vagal afferents in the hindbrain was studied by fluorescent staining against isolectin 4 (IB4). The density of Iba1- and IB4-immunoreactivity was analyzed using Nikon Elements software. There was no difference in the number of FB-labeled neurons located in NG and DMV between VSG and VSG-sham rats. RYGB, but not RYGB-sham rats, showed a dramatic reduction in number of FB-labeled neurons located in the NG and DMV. VSG increased, while the RYGB operation decreased, the density of vagal afferents in the nucleus tractus solitarius (NTS). The RYGB operation, but not the VSG procedure, significantly activated microglia in the NTS and DMV. Results of this study show that the RYGB, but not the VSG procedure, triggers microglia activation in vagal structures and remodels gut-brain communication.
    02/2015; 2015:1-9. DOI:10.1155/2015/601985
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    • "Instead, RYGB mice remain weight neutral due to an increased maintenance metabolic requirement. An understanding of these effects has implications for the development of adjunctive therapy for patients undergoing RYGB aimed at augmenting early postoperative weight loss as well as preventing substantial late post-operative weight regain by offsetting the associated increase in feeding [52] [53]. "
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    ABSTRACT: Glucagon-like peptide-1 (GLP-1) secretion is greatly enhanced after Roux-en-Y gastric bypass (RYGB). While intact GLP-1exerts its metabolic effects via the classical GLP-1 receptor (GLP-1R), proteolytic processing of circulating GLP-1 yields metabolites such as GLP-1(9–36)amide/GLP-1(28–36)amide, that exert similar effects independent of the classical GLP-1R. We investigated the hypothesis that GLP-1, acting via these metabolites or through its known receptor, is required for the beneficial effects of RYGB using two models of functional GLP-1 deficiency – α-gustducin-deficient (α-Gust−/−) mice, which exhibit attenuated nutrient-stimulated GLP-1 secretion, and GLP-1R-deficient mice. We show that the effect of RYGB to enhance glucose-stimulated GLP-1 secretion was greatly attenuated in α-Gust−/− mice. In both genetic models, RYGB reduced body weight and improved glucose homeostasis to levels observed in lean control mice. Therefore, GLP-1, acting through its classical GLP-1R or its bioactive metabolites, does not seem to be involved in the effects of RYGB on body weight and glucose homeostasis.
    Molecular Metabolism 11/2013; 3(2). DOI:10.1016/j.molmet.2013.11.010
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    • "Cre) BAC of Na v 1.8 locus containing Cre β-gal Agarwal et al., 2004 Phox2b cre BAC containing Cre inserted in Phox2b exon 2 YFP All autonomic neurons but sympathetic preganglionic D' Autreaux et al., 2011 Phox2b-Cre BAC containing Cre inserted in Phox2b exon 1 EGFP DMV and NTS Gong et al., 2003 Phox2b-Cre Cre driven by Phox2b with >75 kb at 3 and 5 ends GFP, β-gal, tdTomato DMV, NG, subset of NTS and enteric neurons Rossi et al., 2011; Scott et al., 2011; Gautron et al., 2013b "
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    ABSTRACT: Neurons residing in the gut-brain axis remain understudied despite their important role in coordinating metabolic functions. This lack of knowledge is observed, in part, because labeling gut-brain axis neurons and their connections using conventional neuroanatomical methods is inherently challenging. This article summarizes genetic approaches that enable the labeling of distinct populations of gut-brain axis neurons in living laboratory rodents. In particular, we review the respective strengths and limitations of currently available genetic and viral approaches that permit the marking of gut-brain axis neurons without the need for antibodies or conventional neurotropic tracers. Finally, we discuss how these methodological advances are progressively transforming the study of the healthy and diseased gut-brain axis in the context of its role in chronic metabolic diseases, including diabetes and obesity.
    Frontiers in Neuroscience 07/2013; 7(7):134. DOI:10.3389/fnins.2013.00134 · 3.66 Impact Factor
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