Duodenoileal Interposition    :

1. 1. Duodenum is transected and 100 % excluded from food.
   2. Strong FOREGUT SUPRESSION!
   3. The ileum is connected to post-pyloric duodenum.
   4. Strong HINDGUT STIMULATION!
   5. ERCP becomes impossible due to anatomical exclusion of duodenum!
   6. Its almost Irreversable.
   7. The Most Potent Anti-Diabetic Effect!

Duodenoileal Interposition (DII)

Duodenoileal Interposition (DII) is the first metabolic surgery that was specifically designed to treat Type 2 Diabetes (T2DM) patients with BMI<35 kg/m² by Dr. Aureo Ludovico De Paula from Brazil in 2006. It is almost a “non-malabsorptive” procedure diverting the food to the 40-50 cm of Treitz, to proximal jejunum. This is just the same as standart Roux-en-Y Gastric Bypass (RYGB). But in RYGB food is transfered to the jejunum directly and ileum is still all the way down the whole intestinal length. In this way, RYGB is 100 % a “Foregut” surgery, but stimulation of hindgut is weak. Where as Duodenoileal Interposition (DII) brings the very distal ileal segment to the exit of stomach to have a potent hindgut stimulation. As the duodenum is transected and anatomically excluded, Duodenoileal Interposition (DII) has also a potent effect on “foregut” suppression of negative incretins.

Duodenoileal Interposition (DII) : The Metabolic Effect

Duodenoileal Interposition (DII) is the most potent anti-diabetic surgery with strong foregut suppression and hindgut stimulation. More over, it is as non-malabsorptive as gastric bypass, excluding only duodenum and the first 40 to 50 cm of jejunum.

• Duodenoileal Interposition(DII): Mechanisms of Action

Duodenal Exclusion (FOREGUT SUPRESSION)

Duodenum is the very first part of small intestines and has strong bonds with vital neighbour structures such as pancreas, biliary tract, hepatopancreatic vessels. It is the main part that digestion starts. The food meets at first sight, the biliary-pancreatic juice in duodenum and carbs start to be absorbsed.

Besides these digestive functions, duodenum has important regulatory hormonal effects on the energy metabolism. The negative incretins, normally balance the over-extending effect of first phase insülin reaction to absorption of glucose to inhibit life-treatening hypoglycemia. But in diabetes condition, altough the body resist the insülin hormone (leading to inefficient control of blood sugar), the the negative incretin effect of duodenum stays still and supresses more the defected insülin response. This leads to progression of diabetes. This phenomenon is called The Foregut Effect.

Duodenoileal Interposition (DII) anatomically excludes duodenum from pylorus just as the Duodenal Switch procedure. By this anatomical exclusion of duodenum, the negative incretin effect is definitely suppressed. Therefore Duodenoileal Interposition (DII) is a potent FOREGUT SUPRESSION effect.

Ileal Stimulation. (HINDGUT STIMULATION)

The ileum is the last part of small intestines and is rich in L-cells which is responsible from the secretion of Gulucagonlike Polypeptide 1 (GLP-1) and also PYY. GLP-1 and PYY are called “satiety” hormones.   GLP-1 has spesific effects to support insülin action on the body. It decreases insülin resistance in muscle, liver, brain and kidneys. GLP-1 also decreases beta cell apopitosis (cell deaths) in pancreas and provokes the new beta cell formation.

The most potent HINDGUT Stimulating procedures are the Biliopancreatic Diversion  (BPD) and Duodenal Switch (DS) operations. Duodenoileal Interposition (DII) is as potent as BPD and DS on hindgut stimulation. The undigested food is immediately transferred to very distal ileal segment after pylorus muscle. This is even before it meets the biliopancreatic juice. This early ileal stimulation, provokes strong GLP-1 production and control of the disease.

The Neuro-Endocrine Break

Duodenoileal Interposition (DII) is purely a metabolic surgery. This is because it does not lean on gastric restriction/anastomotic diameter as RYGB and not malabsorptive  as BPD/DS.

Duodenoileal Interposition (DII) can therefore be described as an endocrine surgery which has no anatomical restrictions or malabsorption. It has hormonal targets in all steps. The most potent and prominent one of them is the interposition of ileum. This provokes a sudden and strong GLP-1 stimulation which is proved to be long-lasting over 20 years in similar operations. This GLP-1 secretion effects locally and systematically:

Locally on gastrointestinal system, GLP-1 supresses the motility of the food in digestive system which enhances the feeling of satiety.

Systematically on all targets of insulin hormone such as the muscle cells, liver, brain, kidney and even intestinal mucosa to increase the insulin effects. By this way, especially in brain, the satiety is also provoked. As a sum, after the food is transferred to ileum, the “neuroendocrine effect” immediately takes place and satiety stage is reached. This phenomenon is also called as “The Hormonal Break” or “Neuroendocrine Break”.

The Hormonal Efects: Step by Step

Duodenoileal Interposition (DII) has a hormonal target in all steps of the procedure. Let’s take a look at these.

1. Sleeve Gastrectomy (Removal of Fundus – Gherelin Control)

A weight adjusted sleeve gastrectomy is included as a first step in Duodenoileal Interposition (DII). The sleeve gastrectomy does not aim to restrict the amount of food that can be consumed, but aims to do two main modification:

• To enhance the drainage of stomach to over-come the strong inhibition of gastric motility due to neuroendocrine break.
• To decrease the secretion of gherelin at the beginning. As the ghrelin is a part of the anti-insulinar system, the inhibition of secretion helps to decrease the glucose toxicity of the patient.

1. Duodenal Exclusion

As the duodenum provokes also anti-insulin hormonal secretions, excluion of duodenum naturally stimulates the insülin actions on all over the body. By the duodenal exclusion, the negative incretins are supressed and insülin resistance is decreased.

1. Ileal Interposition

The ileal interposition is the main part of the operation. By the help of this anatomical change, the food ingredient of stomach, can be easily delivered to the very distal part of the small intestines where they can strongly stimulate the L-cells to produce GLP-1 and PYY, the so called satiety hormones. The neuroendocrine break evokes in this way to have local and systematic actions to fix the insülin resistance.

Is Duodenoileal Interposition (DII) malabsorptive?

Totally Non-Malabsorptive Surgery

This is the most important point that we should discuss about Duodenoileal Interposition (DII). Let’s go over again the RYGB (Roux-n-Y Gastric Bypass) which is almost a non-malabsorptive surgery. In RYGB, whole stomach, whole duodenum and up to 50 cm of jejunum are bypassed. The whole intestinal length of a humanbeing might be in between 350 cm to 1100 cm long. So even in the shortest length of bowels (around 350 cm), RYGB can only bypass 1/7^th of the intestines (14.2 % approx.). This means that the 85% of the intestines are in direct contact with food and absorption process. In patients who have longer intestinal lengths, such as 800 cm, the malabsorptive “bypassed” intestinal length gets much more shorter to 1/16^th (6.25 %  approx.) of all the bowels.  That’s why malabsorption becomes neglectable. RYGB patients only needs iron and to some extend B12 replacements as their tiny pouches preserve its volume (40-50 cc approx.). As the pouch enlarges, the patients start to feel more hunger, and feel the increase in portions. Those patients mostly do not need any replacement cause the ingested food becomes available to maintain iron and B12 levels. But this is also related with significant loss of the effect of the RYGB procedure, with weight regain and recurrence of diabetes.

Duodenoileal Interposition (DII) has a similar anatomical bypass comparable with RYGB. Duodenoileal Interposition (DII) also bypasses whole stomach, whole duodenum and up to 50 cm of jejunum. So the malabsorptive compartment is limited to 6-10 % of all bowel length. This is expected to provoke some iron and B12 deficiency but in more than 85 % of DII patients, even these are not present. The main difference is the capacity of stomach to consume. When compared to RYGB pouch of 40-50 cc, the remaining stomach volume of DII is more than 200 cc at the very early post operative period. As the time pass, the stomach volume increases to a capacity more allowing up to almost a meal portion. The impact of the DII does not lean on the stomach restriction and anastomotic diameter as in RYGB. However DII has a strong “neuroendocrine hormonal break” system that provokes hormonal satiety and gastrointestinal motility control which limits the amount of food consumed and triggers insulin sensitivity in all body cells.

Duodenoileal Interposition (DII) has no anatomical limitations on restriction of volume or anastomotic diameter. DII is beyond all of these limitations, acting solely on hormonal issues which enhances by the time as the L-cells increase with early contact with undigested food.