Abstract

ObjectiveBariatric surgery is considered the most efficient treatment for morbid obesity and its related diseases. However, its role as a metabolic modifier is not well understood. We aimed to determine biosignatures of response to bariatric surgery and elucidate short-term metabolic adaptations.MethodsWe used a LC- and FIA-ESI-MS/MS approach to quantify acylcarnitines, (lyso)phosphatidylcholines, sphingomyelins, amino acids, biogenic amines and hexoses in serum samples of subjects with morbid obesity (n = 39) before and 1, 3 and 6 months after bariatric surgery. K-means cluster analysis allowed to distinguish metabotypes of response to bariatric surgery.ResultsFor the first time, global metabolic changes following bariatric surgery independent of the baseline health status of the subjects have been revealed. We identify two metabolic phenotypes (metabotypes) at the interval 6 months-baseline after surgery, which presented differences in the levels of compounds of urea metabolism, gluconeogenic precursors and (lyso)phospholipid particles. Clinically, metabotypes were different in terms of the degree of improvement in insulin resistance, cholesterol, low-density lipoproteins and uric acid independent of the magnitude of weight loss.ConclusionsThis study opens new perspectives and new hypotheses on the metabolic benefits of bariatric surgery and understanding of the biology of obesity and its associated diseases.

Highlights

  • Over the last few decades bariatric surgery has been used as a powerful “disease modifier” for the treatment of morbid obesity, not merely as a strategy for weight loss [1]

  • We identify two metabolic phenotypes at the interval 6 months-baseline after surgery, which presented differences in the levels of compounds of urea metabolism, gluconeogenic precursors and phospholipid particles

  • Metabotypes were different in terms of the degree of improvement in insulin resistance, cholesterol, low-density lipoproteins and uric acid independent of the magnitude of weight loss

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Summary

Introduction

Over the last few decades bariatric surgery has been used as a powerful “disease modifier” for the treatment of morbid obesity, not merely as a strategy for weight loss [1]. Bariatric surgery is the most successful treatment for weight loss, metabolic control and effective prevention, remission or delay of type 2 diabetes progression [2]. The metabolic co-morbidities of obesity such as diabetes improve after bariatric surgery even before weight loss occurs. Unveiling different metabolic fingerprints following bariatric surgery in the earliest stages might help to elucidate the physiological pathways of insulin resistence and the onset of the related co-morbidities

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