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Roles of the gut in the metabolic syndrome: an overview

Journal article
Authors Lars Fändriks
Published in Journal of Internal Medicine
Volume 281
Issue 4
Pages 319-336
ISSN 0954-6820
Publication year 2017
Published at Institute of Clinical Sciences, Section for Surgery and Gastrosurgical Research and Education, Department of Gastrosurgical Research and Education
Pages 319-336
Language English
Links 10.1111/joim.12584
Keywords body weight, chylomicrons, energy expenditure, food intake, glycaemia, metabolism, y gastric bypass, vertical banded gastroplasty, cardiovascular, risk-factors, randomized clinical-trial, intestinal immune-system, glucagon-like peptide-1, bile-acid receptors, bariatric surgery, insulin-resistance, gastrointestinal-tract
Subject categories Gastroenterology and Hepatology

Abstract

The metabolic syndrome is a cluster of risk factors (central obesity, hyperglycaemia, dyslipidaemia and arterial hypertension), indicating an increased risk of diabetes, cardiovascular disease and premature mortality. The gastrointestinal tract is seldom discussed as an organ system of principal importance for metabolic diseases. The present overview connects various metabolic research lines into an integrative physiological context in which the gastrointestinal tract is included. Strong evidence for the involvement of the gut in the metabolic syndrome derives from the powerful effects of weight-reducing (bariatric) gastrointestinal surgery. In fact, gastrointestinal surgery is now recommended as a standard treatment option for type 2 diabetes in obesity. Several gut-related mechanisms that potentially contribute to the metabolic syndrome will be presented. Obesity can be caused by hampered release of satiety-signalling gut hormones, reduced meal-associated energy expenditure and microbiota-assisted harvest of energy from nondigestible food ingredients. Adiposity per se is a well-established risk factor for hyperglycaemia. In addition, a leaky gut mucosa can trigger systemic inflammation mediating peripheral insulin resistance that together with a blunted incretin response aggravates the hyperglycaemic state. The intestinal microbiota is strongly associated with obesity and the related metabolic disease states, although the mechanisms involved remain unclear. Enterorenal signalling has been suggested to be involved in the pathophysiology of hypertension and postprandial triglyceride-rich chylomicrons; in addition, intestinal cholesterol metabolism probably contributes to atherosclerosis. It is likely that in the future, the metabolic syndrome will be treated according to novel pharmacological principles interfering with gastrointestinal functionality.

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