New Data on Weight Gain Following Bariatric Surgery

Gastric bypass surgery has long been considered the gold standard for weight loss. However, recent studies have revealed that this particular operation can lead to potential weight gain years later. Lenox Hill Hospital’s Chief of Bariatric Surgery, Mitchell Roslin, MD, was the principal investigator of the Restore Trial – a national ten center study investigating whether an endoscopic suturing procedure to reduce the size of the opening between the gastric pouch of the bypass and the intestine could be used to control weight gain in patients following gastric bypass surgery. The concept for the trial originated when Dr. Roslin noticed a pattern of weight gain with a significant number of his patients, years following gastric bypass surgery. While many patients could still eat less than before the surgery and become full faster, they would rapidly become hungry and feel light headed, especially after consuming simple carbohydrates, which stimulate insulin production.

The results of the Restore Trial, which were published in January 2011, did not confirm the original hypothesis – there was no statistical advantage for those treated with suturing. However, they revealed something even more important. The data gathered during the trial and the subsequent glucose tolerance testing verified that patients who underwent gastric bypass surgery and regained weight were highly likely to have reactive hypoglycemia, a condition in which blood glucose drops below the normal level, one to two hours after ingesting a meal high in carbs. Dr. Roslin and his colleagues theorized that the rapid rise in blood sugar – followed by a swift exaggerated plunge – was caused by the absence of the pyloric valve, a heavy ring of muscle that regulates the rate at which food is released from the stomach into the small intestine. The removal of the pyloric valve during gastric bypass surgery causes changes in glucose regulation that lead to inter-meal hunger, impulse-snacking, and consequent weight regain.

Dr. Roslin and his team decided to investigate whether two other bariatric procedures that preserve the pyloric valve – sleeve gastrectomy and duodenal switch – would lead to better glucose regulation, thus suppressing weight regain. The preliminary data of this current study shows that all three operations initially reduce fasting insulin and glucose. However, when sugar and simple carbs are consumed, gastric bypass patients have a 20-fold increase in insulin production at six months, compared to a 4-fold increase in patients who have undergone either a sleeve gastrectomy or a duodenal switch procedure. The dramatic rise in insulin in gastric bypass patients causes a rapid drop in glucose, promoting hunger and leading to increased food consumption.

“Based on these results, I believe that bariatric procedures that preserve the pyloric valve lead to better physiologic glucose regulation and ultimately more successful long-term maintenance of weight-loss,” said Dr. Roslin.

Claudia Cheng

updated in August 2006

Introduction

Stomach emptying is a coordinated function by intense peristaltic contractions in the antrum. At the same time, the emptying is opposed by varying degrees of resistance to passage of chyme at the pylorus. Rate depends on pressure generated by antrum against pylorus resistance. Chyme = food in stomach which has been thoroughly mixed with stomach secretions

Factors affecting stomach empyting

1. Promote

§         Gastric volume

o       Increased food volume in stomach promotes increased emptying

o       Antral distension stimulates vasovagal excitatory reflexes leading to increased antral pump activity

§         Liquid vs solid food

o       Pylorus is open enough for H2O/fluids to empty with ease. Constriction of the pyloric sphincter to solids until chyme is broken down into small particles and mixed  to almost fluid consistency

§         Types of food

o       Protein empties fastest, followed by carbohydrates. Fats take longest to empty

o       Note: high protein food especially meat stimulate release of gastrin from antral mucosa

§         Hormonal factors

o       Gastrin has mild to moderate stimulatory effects on motor functions in the body of the stomach. Enhances activity of pyloric pump

o       Motilin released by epithelium of the small intestine enhances the strength of the migrating motor complex which is a peristaltic wave that begins within the oesophagus and travels thru the whole GIT every 60-90 min during the interdigestive period. Help empty remaining food in stomach

§         Neural

o       Parasympathetic innervation (via vagus) stimulates motility

o       Local myenteric reflex

§         Drugs

o       Prokinetics eg cisapride, erythromycin metoclopramide

2. Inhibit

§         Duodenal distension

o       Results in inhibitory enterogastic reflexes

o       Slow or even stop stomach emptying if the volume of chyme in the duodenum becomes too much

§         Osmolarity of chyme

o       Iso-osmotic gastric contents empty faster than hyper or hypo-osmotic contents due to feedback inhibition produced by duodenal chemoreceptors (hyper more inhibitory than hypo)

§         Types of food

o       Fat and protein breakdown products in the small intestine inhibits gastric emptying

§         Acid

o       pH of chyme in the small intestine of < 3.5-4 will activate reflexes to inhibit stomach emptying until duodenal chyme can be neutralized by pancreatic and other secretions

§         Temperature

o       Cold liquid (4⁰C) empty more slowly

§         Hormones

o       Cholecystokinin released from duodenum in response to breakdown products of fat and protein digestion. Blocks the stimulatory effects of gastrin on the antral smooth muscle

o       Secretin released from the duodenum in response to acid, has a direct inhibitory effect on the gastric smooth muscles

o       Others eg somatostatin, vasoactive intestinal peptide (VIP), gastic inhibitory peptide (GIP)

§         Neural

o       Sympathetic nerves (via the celiac plexus) inhibits motility

§         Patient factors

o       Pregnancy delays gastric emptying (progesterone)

o       Anxiety delays gastric emptying

o       Pain

o       Elderly

o       Disease states eg diabetes mellitus (autonomic neuropathy), post-operative bowel surgery with resultant ileus, high intra-abdominal pressure

§         Drugs  eg. opioids

§         Mechanical eg pyloric stenosis

 Ó Claudia Cheng August 2006

http://www.britannica.com/EBchecked/topic/484656/pylorus?anchor=ref237588
pylorus, 
cone-shaped constriction in the gastrointestinal tract that demarcates the end of the stomach and the beginning of the small intestine. The main functions of the pylorus are to prevent intestinal contents from reentering the stomach when the small intestine contracts and to limit the passage of large food particles or undigested material into the intestine.

The internal surface of the pylorus is covered with a mucous-membrane lining that secretes gastric juices. Beneath the lining, circular muscletissue allows the pyloric sphincter to open or close, permitting food to pass or be retained. 


 

What is gastric emptying?

Gastric emptying is the process by which the stomach empties its contents into the duodenum of the small intestine for further digestion of food and absorption of nutrients. While this may seem like a simple process, it is carefully coordinated so as not to overwhelm the duodenum with large amounts of partially digested food mixed with the acidic gastric secretions, which is collectively known as chyme.

The stomach is a muscular, hollow organ. When food enters the stomach, it is churned by the stomach contractions (peristalsis) with gastric secretions (refer to Gastric Acid Secretion) and this allows for both mechanical and chemical digestion. Most of this churning occurs within the body of the stomach where the muscle contractions are weak.

The contractions lower down the stomach, near the pylorus, are more intense. This pushes the more fluid chyme through the pylorus while undigested food particles are forced higher up into the stomach for further breakdown. These stronger peristaltic waves that occur near the pylorus propel the fluid chyme through the pylorus into the duodenum in a pump-like action. This is referred to as the ‘pyloric pump‘.

The distal part of pylorus has a thick muscular wall arranged in a circular manner which remains contracted in a normal state. This is known as the pyloric sphincter. Even though it is contracted, the sphincter is not totally closed and there is gap which allows fluids like water or chyme to move through into the duodenum but prevents the movement of larger food particles.

What promotes or inhibits gastric emptying?

The vagus nerve is mainly responsible for parasympathetic stimulation to the stomach. This increases peristalsis and opens the pyloric sphincter. Sympathetic stimulation via the celiac plexus inhibits peristalsis and the opening of the sphincter. This is influenced by brain stem as well as stimuli from the sensory nerve endings in the gastric epithelium. Refer to Stomach Nerves for more information on the stomach nerve supply.

Causes

Stomach and pyloric valve

In dumping syndrome, food and gastric juices from your stomach move to your small intestine in an unregulated, abnormally fast manner. This accelerated process is most often related to changes in your stomach associated with surgery. For example, when the opening (pylorus) between your stomach and the first portion of the small intestine (duodenum) has been damaged or removed during an operation, dumping syndrome may develop.

Dumping syndrome may occur at least mildly in one-quarter to one-half of people who have had gastric bypass surgery. It develops most commonly within weeks after surgery, or as soon as you return to your normal diet. The more stomach removed or bypassed, the more likely that the condition will be severe. It sometimes becomes a chronic disorder.

Gastrointestinal hormones also are believed to play a role in this rapid dumping process.


http://emedicine.medscape.com/article/173594-overview

 

Background

The stomach serves as the receptive and storage site of ingested food. The primary functions of the stomach are to act as a reservoir, to initiate the digestive process, and to release its contents downstream into the duodenum in a controlled fashion. The capacity of the stomach in adults is approximately 1.5-2 liters, and its location in the abdomen allows for considerable distensibility. Gastric motility is regulated by the enteric nervous system, which is influenced by extrinsic innervation and by circulating hormones. Alterations in gastric anatomy after surgery or interference in its extrinsic innervation (vagotomy) may have profound effects on gastric emptying. These effects, for convenience, have been termed postgastrectomy syndromes.

Postgastrectomy syndromes include small capacity, dumping, bile gastritis, afferent loop syndrome, efferent loop syndrome, anemia, and metabolic bone disease. Postgastrectomy syndromes are iatrogenic conditions which may arise from partial gastrectomies, independent of whether the gastric surgery was initially done for peptic ulcer disease, cancer, or for weight loss (bariatric). The surgical procedures include Billroth-I, Billroth-II, and Roux-en-Y.¹

Pathophysiology

Dumping is the effect of altered gastric reservoir function, and abdominal postoperative gastric motor function.²The early dumping syndrome and reflux gastritis are less frequent when segmented gastrectomy rather than distal gastrectomy is performed for early gastric cancer.³ In persons with long segment Barrett esophagus treated with a truncal vagotomy, partial gastrectomy, plus Roux-en-Y gastrojejunostomy, 41% developed dumping within the first 6 months after surgery, but severe dumping is rare (5% of cases).⁴ 

The dumping syndrome occurs in 45% of persons who are malnourished and who have had a partial or complete gastrectomy.⁵ The late dumping syndrome is suspected in the person who has symptoms of hypoglycemia in the setting of previous gastric surgery, and this late dumping can be proven with an oral glucose tolerance test (hyperinsulinemic hypoglycemia), as well as gastric emptying scintigraphy that shows the abnormal pattern of initially delayed and then accelerated gastric emptying.⁶ 

Clinically significant dumping syndrome occurs in approximately 10% of patients after any type of gastric surgery. Dumping syndrome has characteristic alimentary and systemic manifestations. It is the most common and often disabling postprandial syndrome observed after a variety of gastric surgical procedures, such as vagotomy, pyloroplasty, gastrojejunostomy, and laparoscopic Nissan fundoplication. Dumping syndrome can be separated into early and late forms, depending on the occurrence of symptoms in relation to the time elapsed after a meal. Both forms occur because of rapid delivery of large amounts of osmotically active solids and liquids into the duodenum. Dumping syndrome is the direct result of alterations in the storage function of the stomach and/or the pyloric emptying mechanism.

Pathophysiology of dumping syndrome.

Gastric resection reduces the fundic reservoir, thereby reducing the stomach's receptiveness (accommodation) to a meal. Vagotomy increases gastric tone, similarly limiting accommodation. An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric emptying. Duodenal feedback inhibition of gastric emptying is lost after a bypass procedure, such as gastrojejunostomy. Accelerated gastric emptying of liquids is a characteristic feature and a critical step in the pathogenesis of dumping syndrome. Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of digestion are affected adversely. All these factors interplay in the pathophysiology of dumping syndrome.