Dumping Dependent Diabetes: Surgical Paradigm

This ongoing column is dedicated to sharing with readers the life and experiences of Dr. Edward Mason

Column Editor: Tracy Martinez, RN, BSN, CBN
Ms. Martinez is the Program Director for Wittgrove Bariatric Center in La Jolla, California.

This month: Dumping Dependent Diabetes: Surgical Paradigm

Bariatric Times. 2013;10(11):12.

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No one has asked a very important question: Should we not consider type 2 diabetes (T2D) as a disease of the digestive tract? The following would be my support.

In 1998, Näslund et al1 wrote about the importance of GLP-1 in continued improvement of glucose metabolism 20 years after intestinal bypass for obesity. In 1999 I suggested studying a laboratory model of moving the ileum to a position close to the duodenum to determine whether this would stimulate the secretion of GLP-1.2 Strader et al[3] performed this study in rodents and found a postprandial increase in GLP-1 secretion, which supported dumping as the mechanism whereby glucose and other stimulants of L cell secretion reach the ileum early in a meal after gastric bypass.

If dumping is required to resolve T2D then we must all dump or we would have T2D.  Brener et al observed that initial emptying of the stomach during a meal is governed by the volume of stomach contents and is a gush that overflows the duodenum, where gastric contents are normally diluted by bile and pancreatic juice.4 Such highly concentrated contents are irritating. This initiates flushing to the distal bowel like the hyperosmotic cathartic, milk of magnesia. Glucose and other stimulants of GLP-1 secretion thus reach the ileum L cells early during a meal. This normal dumping is usually without symptoms.  In normal people and after the initial gastric gush/flush, emptying squirts are regulated by glucose receptors and other receptors in the duodenum to provide a diluted, non-irritating content for entrance into the jejunum at a rate that assists in maintaining normal plasma glucose concentration.  Dumping is the way our digestive tract is programmed early in a meal and reprogrammed when the concentration of stomach content is changed by additional intake.

In both Billroth-2 and Roux-en-Y reconstructions most of the stomach and the entire duodenum are bypassed. The swallowed highly concentrated content passes directly into the jejunum and stimulates rapid transit to the ileum where GLP-1 secretion is stimulated along with other hormones of L cells. The only difference between the Billroth loop and Roux-en-Y reconstruction is where the digestive juices enter the jejunum. The Billroth loop allows these digestive juices to enter the stomach pouch at the confluence of the Y. The Roux-en-Y has these juices entering at a lower level so that they will not reach the stomach pouch.
Most of the stomach is in the left upper limb along with the duodenum in both bypass operations. The left bypassed limb and the right stomach pouch limb join the common limb at the stomach pouch with Billroth’s bypass operation. This allows bile and pancreatic digestive juice to enter the stomach pouch. In RYGB the left Y limb enters the confluence at a lower level of the jejunum so that bile and pancreatic juice does not enter the stomach pouch and cause heart burn. Both operations expose the upper small bowel to highly concentrated contents and cause concentrated (hypertonic and hyperosmotic) flushing/dumping. The Roux reconstruction divides the bilio-pancreatic limb at the confluence and attaches it at a lower level of the jejunum to keep the irritating bile and other digestive juices away from refluxing into the stomach pouch and esophagus. The site of exposure of jejunum to highly concentrated contents remains where the stomach pouch empties into small bowel. This is where dumping begins and is next to the stomach pouch in bypass operations.

T2D appears to be a disease of digestive tract dysfunction in which there is no gastric emptying gush and no flush. The operations that cause immediate resolution of T2D are those that result in immediate dumping and immediate elevation of plasma GLP-1 after the highly concentrated fluid is swallowed. We seldom swallow solid food.  It is converted to liquid by chewing and mixing with saliva. In the Hela monster from the time of dinosaurs the GLP-1 like hormone is present in saliva and enters both the blood stream and digestive tract at meal time. It appears that an evolutionary movement occurred of GLP-1 type secreting cells from an ancient lizard’s salivary glands to become distal bowel L cells.5

It has taken a century to recognize the surgical mechanism for prevention and treatment of T2D. Bypass surgery has shown a way to prevent and resolve T2D in the epidemic without surgery when obesity is less severe. GLP-1 related treatment is available and glucose mimetic therapy should be possible.

References
1.    Näslund E, Backman L, Holst JJ, et al. Importance of small bowel peptides for the improved glucose metabolism 20 years after jejunoileal bypass for obesity. Obes Surg. 1998;8:253–260.
2.    Mason EE. Ileal transposition and enteroglucagon/GLP-1 in obesity (and diabetic?) surgery. Obes Surg. 1999; 9:223–228.
3.    Strader A D, Torsten P V, Ronald JJ, et al. Weight loss through ileal transposition is accompanied by increased ileal hormone secretion and synthesis in rats. Am J Physiol Endocrinol Metab. 2005; 288:E447–E453.
4.    Brener W, Hendrix TR, McHugh PR. Regulation of the gastric emptying of glucose. Gastroenterololgy. 1983; 85:76–82.
5.    Mason EE. Gila Monster’s Guide to Surgery for Obesity and Diabetes. J Am Coll Surg. 2008; 206: 357–360.

Category: Ed Mason at Large, Past Articles