Treatment of Type 2 Diabetes Mellitus by Duodenal Exclusion Associated With Omentectomy: Clinical and Hormonal Study
Treatment of Type 2 Diabetes Mellitus by Duodenal Exclusion Associated With Omentectomy: Clinical and Hormonal Study
Based in a surgery technique studied in a non-obese diabetic mouse model by Rubino and
 Marescaux(2004), wich reversed diabetes in those animals, we have performed a previous study
 in human volunteers with type 2 diabetes and overweight (non-obese). The surgery is a
 duodenal exclusion in wich the stomach volume is kept intact. We observed improvement of
 glycemic control and hemoglobin A1c, allied to reduction of medicines: insulin was withdrawn
 or significantly lowered.

 Further improvement of diabetes could be achieved by intervention in insulin resistance,
 another factor of diabetes pathophysiology. As that factor is related to visceral fat, we
 hypothesize that surgical removal of the major omentum, a great component of central
 adiposity, could beneficial .

 This study will evaluate the mechanisms of amelioration of type 2 diabetes mellitus after
 duodenal exclusion surgery plus total omentectomy, by the method of standardized meal
 stimulus and insulin tolerance test, in human non-obese volunteers with diabetes type 2 and
 known insulin secretion capacity.

 The previously studied volunteers submitted to duodenal exclusion without omentectomy will be
 the control group.
Diabetes reversion is observed after bariatric surgeries even before significant weight loss
 could explain it, mainly in predominantly malabsorptive procedures, followed by those
 combining malabsorption and gastric restriction. Changes in the hormonal communication
 between the digestive system (incretins)and the pancreas would explain the antidiabetogenic
 role of the surgery, so this effect could be obtained in nonobese, diabetic individuals.

 Based in a surgery technique studied in a non-obese diabetic mouse model by Rubino and
 Marescaux(2004), wich reversed diabetes in those animals, we have performed a previous study
 in human volunteers with type 2 diabetes and overweight (non-obese). The surgery is a
 duodenal exclusion: the stomach volume is kept intact, maintaining the caloric ingestion and
 the weight reduces less than 5%, without the potential nutritional deprivations commonly seen
 in the bariatric surgery. We observed improvement of glycemic control and hemoglobin A1c,
 allied to reduction of medicines: insulin was withdrawn or significantly lowered. An
 standardized mixed meal tolerance test showed favorable changes in the gastrointestinal
 hormones that stimulate insulin secretion (incretins): increase of GLP-1 and reduction of
 GIP.

 Further improvement of diabetes could be achieved by intervention in insulin resistance,
 another factor of diabetes pathophysiology. As that factor is related to visceral fat, we
 hypothesize that surgical removal of the major omentum, a great component of central
 adiposity, could beneficial .

 In fact, surgical removal of visceral fat in rodents improves insulin sensitivity. A pilot
 study in human, obese volunteers submitted to gastric adjustable band was promising int this
 aspect.

 This study will evaluate the mechanisms of amelioration of type 2 diabetes mellitus after
 duodenal exclusion surgery plus total omentectomy , by the method of standardized meal
 stimulus and insulin tolerance test, in human non-obese, volunteers with diabetes type 2 and
 known insulin secretion capacity.

 The previously studied volunteers submitted to duodenal exclusion without omentectomy will be
 the control group.
Inclusion Criteria:

 -  Age: 18 to 60 years.

 -  BMI between 25 and 29,9 kg/m².

 -  Weight variance less than 5% in the last 3 months.

 -  Previous diagnosis of diabetes type 2.

 -  Insulin requirement, alone or along with oral agents

 -  Capacity to understand the procedures of the study.

 -  To agree voluntarily to participate of the study, signing an informed consent.

 Exclusion Criteria:

 -  Positive Anti-GAD antibodies

 -  Laboratorial signal of probable failure of insulin production, i. e., seric peptide C
 lesser than 1 ng/mL.

 -  History of hepatic disease like cirrhosis or chronic active hepatitis.

 -  Kidney dysfunction (creatinine > 1,4 mg/dl in women and > 1,5 mg/dl in men).

 -  Hepatic dysfunction: ALT and/or AST 3x above upper normal limit.

 -  Recent history of neoplasia (< 5 years).

 -  Use of oral or injectable corticosteroids for more than consecutive 14 days in the
 last three months.