Bariatric surgery

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Introduction

Surgery as a treatment for obesity

For many obese patients, diets and lifestlye changes do not work in long term. Bariatric surgery has proved to be the only effective method in the long term treatment of obesity.

How surgery works

Bariatric surgery works by altering the anatomy of the gastrointestinal tract, thus: limiting the volume of food the stomach can hold, interfering with the absorption of calories, and by interfering with orexigenic and anorexigenic signalling between the gut, adipose tissues and the brain.

Bariatric Surgical Procedures

Restrictive Surgery

Restrictive surgery reduces the size of the stomach causing decreased hunger and an increased satiety following ingestion of smaller amounts of food. Surgical procedures include gastric banding, where an adjustable band is clipped just below the cardia of the stomach creating a small gastric pouch above(kerrigan, le roux). Other forms of restrictive surgery includes gastroplasty and sleeve gasrectomy.

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Malabsorptive Surgery

Jejuno-ileal bypass, duodenojejunal bypass and biolopancreatic bypass (with or without duodenal switch)

Combination Surgery

Combination surgery combines the benefits of both restrictive and restrictive surgery. The most common bariatric procedure in the US is the Roux-en-Y Gastric Bypass (RYGP).

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Duodenal switch

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Surgical Effects Regarding Gut Hormones

Figure 4. Bariatric surgery works by altering appetite though modulation of both gut hormones via the gut-brain axis and the adipose hormones via the adipose-brain axis. Restrictive surgery (gastric banding and sleeve gastrectomy) reduce the size of the forgut. Forgut bypass surgery (Gastric bypass and biliopancreatic diverson) bypasses anatomical segments of the stomach and duodenum (forgut) exposing the hindgut. Midgut bypass surgery (jejuno-ileal bypass) bypasses anatomical segments of the jejunum and ileum, exposing the hindgut.

Hindgut Hormones

Peptide tryosine tryosine (PYY) is a peptide beloging to the neuropeptide Y (NPY) family (broberger). PYY is normally released in proportion to carolie intake and has recently been described as an important feedback molecule in the Gut-Brain axis. Following bypass and restrictive surgerys, basal and postprandial PYY levels have been shown to incease (Ashrafian). In addition basal PYY levels have been shown to increase following illial resection and patients have been reported to have lost weight(broberger). As well as being a satiety signal PPY has also been suggested to increase energy expendature(murphy).

Glucagon-like peptide-1 (GLP-1), acts similarly to PYY, acting in the hypothalamus as an anorexigenic signal. The literature shows the majority of patients following foregut bypass surgery show a marked increase in basal and postprandial GLP-1. Midgut bypass also shows an increase in GLP-1 however studies on restrictive surgery have shown either no change or a decrease in GLP-1 basal levels. Of specific interest GLP-1 has been shown to improve postpriandal glycaemic control, being a potent incretin mimetic. A GLP-1 agonist, exenatide has not yet been accepted for use as an anti-obesity drug; however it is already being used in the treatment of type 2 diabetes mellitus.

Midgut Hormones

Neurotensin (NT), is a well know anoregigenic signal where its expression has been shown to be downregulated in ob/ob leptin defficient mice. Following bypass surgerys (5 of 6 reported) have demonstrated an increase in NT levels which could contribute to the anorexigenic effects of the bypass operations.

Foregut Hormones

Ghrelin, Cholecystokinin, Gastrin