Abstract

Previous studies have shown that Roux‑en‑Y gastric bypass (RYGB), one of the most effective weight loss treatments for obesity, results in neurodegenerative responses in vagal afferent gut‑brain connection reflected by microglia activation and reduced sensory input to the nucleus tractus solitarius (NTS). However, it is not known whether RYGB‑induced microglia activation is the cause or an effect of the reported neuronal damage. Therefore, the aim of this study was to establish the order of neurodegenerative responses in vagal afferents after RYGB in the nodose ganglia (NG) and NTS in male and female rats. Sprague‑Dawley rats were fed regular chow or an energy‑dense diet for two weeks followed by RYGB or sham surgery. Twenty‑four hours later, animals were sacrificed and NG and NTS were collected. Neuronal cell damage was determined by TUNEL assay. Microglia activation was determined by quantifying the fluorescent staining against the ionizing calcium adapter‑binding molecule 1. Reorganization of vagal afferents was evaluated by fluorescent staining against isolectin 4. Results of the study revealed significantly increased DNA fragmentation in vagal neurons in the NG when observed at 24 h after RYGB. The surgery did not produce rapid changes in the density of vagal afferents and microglia activation in the NTS. These data indicate that decreased density of vagal afferents and increased microglia activation in the NTS likely ensue as a res ult of RYGB‑induced neuronal damage.

Highlights

  • In 2016, the prevalence of obesity was 39.8% in adults and 18.5% among children and adolescents in the United States (Hales et al, 2017)

  • The current study revealed that partial damage to vagal afferents by Roux‐en‐Y gastric bypass (RYGB) surgery triggered a significant increase in DNA fragmentation, a marker of apoptosis, in vagal neurons located in the nodose ganglia (NG) within 24 h

  • We show that RYGB induced rapid and signifi‐ cant DNA fragmentation in the NG in male and female rats

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Summary

Introduction

In 2016, the prevalence of obesity was 39.8% in adults and 18.5% among children and adolescents in the United States (Hales et al, 2017). More than 1/3 of adults are overweight or obese (Engin, 2017). Chronic inflammato‐ ry disease associated with increased risk of developing metabolic syndrome, cardiovascular disease, and type II diabetes (Heron, 2018). Even though the hormonal changes following bariat‐ ric surgery are well understood (Meek et al, 2016; Al‐ amuddin et al, 2017), its effects on reorganization of the vagal gut‐brain connections are largely unknown (Gautron et al, 2013). Understanding neuroanatomical changes that underlie the beneficial weight‐loss effect and/or other side effects of bariatric surgery is of para‐ mount importance for the development of non‐surgical therapeutic procedures

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