Abstract

We determined whether persistent nausea and vomiting (N/V) symptoms following Roux-en-Y gastric bypass surgery is due to elevated systemic glucagon-like peptide-1 (GLP-1) and leptin in female non-diabetic subjects. Subjects with N/V post-Roux-en-Y gastric bypass (RYGB) surgery had significantly elevated fasting GLP-1 levels compared to that with post-operative asymptomatic subjects and to morbidly obese, obese and lean subjects not undergoing surgery. Weight loss, glycaemia, insulin and post-prandial GLP-1 levels were similar in all post-operative subjects. Despite comparable BMI, leptin was significantly lower in symptomatic subjects. Furthermore, leptin secretion from subcutaneous adipose tissue was inhibited by GLP-1 (0.1–1.0 nM; n = 6). Persistent N/V following RYGB surgery is associated with elevated fasting GLP-1, but lower leptin levels. The latter may be a consequence of the direct GLP-1 inhibition of leptin secretion from adipose tissue.

Highlights

  • Bariatric surgery is to date the only intervention that results in significant and sustained weight loss for morbid obesity [1]

  • Fasting plasma Glucagon-like peptide-1 (GLP-1) levels were significantly higher in the subjects with persistent nausea and vomiting (N/V) post-Roux-en-Y gastric bypass (RYGB) surgery compared to all other groups (P=0.007, Fig. 1b(i))

  • N/V is a common side effect experienced by the majority of patients undergoing RYGB, but symptoms usually disappear shortly after the operation [12]

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Summary

Introduction

Bariatric surgery is to date the only intervention that results in significant and sustained weight loss for morbid obesity [1]. Procedures such as Roux-en-Y gastric bypass (RYGB), which combines gastric restriction with the bypass of the stomach and proximal intestine, are more effective than other forms of metabolic surgery [1]. GLP-1 infusions reduce energy intake in lean and overweight subjects [4]. Endogenous GLP-1 appears to reduce food intake by acting in a paracrine-like fashion on adjacent GLP-1 receptors (GLP-1R) expressed on vagal afferents innervating the GI tract, rather than acting directly on GLP-1R in the brain [4]

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