Minimally Invasive Procedure Offers Solution to Diabetes, Obesity

An endoscopically implanted gastric liner helps limit uptake by sugar-excreting intestinal bacteria in the stomach and small intestine, which have an important role in the development of metabolic syndrome, diabetes, and obesity.

The EndoBarrier Gastrointestinal Liner System is a nonsurgical therapeutics metabolic treatment that bridges the gap between pharmaceuticals and surgery. Intended for people living with type 2 diabetes, obese people at risk of the disease, and people with severe weight problems, the system offers an effective treatment alternative for those who are unhappy with the current methods of treatment. The device is placed in the gastrointestinal (GI) tract endoscopically via an oral approach, creating a barrier between food and the wall of the intestine.


EndoBarrier placement is an outpatient procedure that takes about 30 minutes to perform, and does not require incisions. The device is simply positioned in the duodenal bulb, and fastened into place with an anchor. When in place, the EndoBarrier lines the small intestine just below the pylorus, creating a physical barrier 60 centimeters in length that prevents food from coming into contact with the intestinal wall, thus preventing the activation of hormonal signals that originate in the intestine. The food thus bypasses the duodenum and proximal jejunum, resulting in an effect similar to that of a Roux-en-Y gastric bypass surgical procedure.

The EndoBarrier is removed after the treatment period—ranging anywhere from three to twelve months in clinical trials. The removal process is another quick (15 minute) and easy endoscopic procedure that is performed using a custom retrieval system. The EndoBarrier Gastrointestinal Liner System is a product of GI Dynamics (Lexington, MA, USA), which has also developed the EndoBarrier Flow Restrictor, a membrane with a small opening that is designed to delay gastric emptying by providing adjustable restriction at the stomach outlet.

The connection between gut microbiota and energy homeostasis and inflammation and its role in the pathogenesis of obesity-related disorders are increasingly recognized. Animal models of obesity connect an altered microbiota composition to the development of obesity, insulin resistance, and diabetes in the host through several mechanisms, including increased energy harvest from the diet, altered fatty acid metabolism and composition in adipose tissue and liver, modulation of gut peptide YY and glucagon-like peptide (GLP)-1 secretion, activation of the lipopolysaccharide toll-like receptor-4 axis, and modulation of intestinal barrier integrity by GLP-2.

Studies also suggest that obesity is associated with a 50% reduction in Bacteroidetes and a proportional division-wide increase in Firmicutes in the distal gut. Besides an increased energy harvest from the diet, further mechanisms linking gut microbiota to obesity have been subsequently proposed, including chronic low-grade endotoxinemia, regulation of biologically active fatty acid composition, and modulation of gut-derived peptide secretion.

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