Sleeve Gastrectomy With Transit Bipartition: A Potent Intervention for Metabolic Syndrome and Obesity

Objective: To present 5-year results of sleeve gastrectomy (SG) with transit bipartition (TB) as a metabolic intervention for obesity. Background: Recent data suggest that high glycemic index foods may lead to a hormonally hyperactive proximal gut and a hypoactivate distal gut, which are linked to metabolic syndrome. TB was designed to counterbalance these effects. Methods: A total of 1020 obese patients with body mass index (BMI) ranging from 33 to 72 Kg/m2 underwent SG and TB (SG + TB). TB creates a gastroileal anastomosis in the antrum after the SG; nutrient transit is maintained in the duodenum, avoiding blind loops and minimizing malabsorption. The stomach retains 2 outflow pathways. A lateral enteroanastomosis connects both segments at 80 cm proximal to the cecum. Results: Adequate follow-up data were collected in 59.1% of patients from 4 months to 5 years. The average percent of excess BMI loss was 91%, 94%, 85%, 78%, and 74% in the first, second, third, fourth, and fifth year, respectively. Patients experienced early satiety and major improvement in presurgical comorbidities, including diabetes (86% in remission), following surgery. Two deaths occurred (0.2%). Other surgical complications occurred in 6% of patients. Signs of malabsorption were rare. Conclusions: SG + TB is a simple procedure that results in rapid weight loss and remission or major improvement of comorbidities. Strictly aiming at physiological correction, TB avoids prostheses, narrow anastomoses, excluded segments, and malabsorption. Weight and comorbidities are much improved. Diabetes is improved without duodenal exclusion. TB is an excellent complement to an SG.

[1]  M. Santo,et al.  Metabolic effects of an entero-omentectomy in mildly obese type 2 diabetes mellitus patients after three years , 2011, Clinics.

[2]  J. Holst,et al.  The separate and combined impact of the intestinal hormones, GIP, GLP-1, and GLP-2, on glucagon secretion in type 2 diabetes. , 2011, American journal of physiology. Endocrinology and metabolism.

[3]  J. Holst,et al.  GIP Does Not Potentiate the Antidiabetic Effects of GLP-1 in Hyperglycemic Patients With Type 2 Diabetes , 2011, Diabetes.

[4]  R. Roberts,et al.  The relationship between postprandial bile acid concentration, GLP‐1, PYY and ghrelin , 2011, Clinical endocrinology.

[5]  D. Damiani,et al.  Bariatric Surgery in Adolescents: Preliminary 1-year Results with a Novel Technique (Santoro III) , 2010, Obesity surgery.

[6]  N. Irwin,et al.  Active immunization against (Pro3)GIP improves metabolic status in high‐fat‐fed mice , 2010, Diabetes, obesity & metabolism.

[7]  J. Holst,et al.  Glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide: new advances , 2010, Current opinion in endocrinology, diabetes, and obesity.

[8]  N. Irwin,et al.  Evidence for beneficial effects of compromised gastric inhibitory polypeptide action in obesity-related diabetes and possible therapeutic implications , 2009, Diabetologia.

[9]  S. Santoro Is the Metabolic Syndrome a Disease of the Foregut? Yes, Excessive Foregut , 2008, Annals of surgery.

[10]  S. Santoro Adaptive and Neuroendocrine Procedures: A New Pathway in Bariatric and Metabolic Surgery , 2008, Obesity surgery.

[11]  D. Damiani,et al.  Digestive Adaptation with Intestinal Reserve: A Neuroendocrine-Based Operation for Morbid Obesity , 2006, Obesity surgery.

[12]  A. Baltasar,et al.  Laparoscopic Sleeve Gastrectomy: A Multi-purpose Bariatric Operation , 2005, Obesity surgery.

[13]  E. Bojanowska Physiology and pathophysiology of glucagon-like peptide-1 (GLP-1): the role of GLP-1 in the pathogenesis of diabetes mellitus, obesity, and stress. , 2005, Medical science monitor : international medical journal of experimental and clinical research.

[14]  Henry Buchwald,et al.  Bariatric surgery: a systematic review and meta-analysis. , 2004, JAMA.

[15]  J. Holst,et al.  Incretin secretion in relation to meal size and body weight in healthy subjects and people with type 1 and type 2 diabetes mellitus. , 2003, The Journal of clinical endocrinology and metabolism.

[16]  Yuichiro Yamada,et al.  Inhibition of gastric inhibitory polypeptide signaling prevents obesity , 2002, Nature Medicine.

[17]  Lambert Nt,et al.  The multifaceted potential of glucagon-like peptide-1 as a therapeutic agent. , 2002 .

[18]  A. Luciani,et al.  Evidence for early impairment of glucagon-like peptide 1-induced insulin secretion in human type 2 (non insulin-dependent) diabetes. , 2002, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.

[19]  N. Vrang,et al.  Glucagon-like peptide containing pathways in the regulation of feeding behaviour , 2001, International Journal of Obesity.

[20]  J. Holst,et al.  Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients. , 2001, Diabetes.

[21]  E. Mason Ilial Transposition and Enteroglucagon/GLP-1 in Obesity (and Diabetic?) Surgery , 1999, Obesity surgery.

[22]  G. Dohm,et al.  A new paradigm for type 2 diabetes mellitus: could it be a disease of the foregut? , 1998, Annals of surgery.

[23]  H. W. Chapman Comparative Physiology of the Vertebrate Digestive System, 2nd ed , 1997 .

[24]  J. Holst,et al.  Gastrointestinal hormones and gastric emptying 20 years after jejunoileal bypass for massive obesity , 1997, International Journal of Obesity.

[25]  V. Marks,et al.  Attenuated GLP-1 secretion in obesity: cause or consequence? , 1996, Gut.

[26]  J. Cuber,et al.  Luminal glucagon-like peptide-1(7-36) amide-releasing factors in the isolated vascularly perfused rat colon. , 1995, The Journal of endocrinology.

[27]  L. Aiello,et al.  The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution , 1995, Current Anthropology.

[28]  C. Johansson,et al.  Gastrointestinal function in obesity: motility, secretion, and absorption following a liquid test meal. , 1992, Metabolism: clinical and experimental.

[29]  V. Marks,et al.  Effect of the entero-pancreatic hormones, gastric inhibitory polypeptide and glucagon-like polypeptide-1(7-36) amide, on fatty acid synthesis in explants of rat adipose tissue. , 1991, The Journal of endocrinology.

[30]  D. Wingate Comparative physiology of the vertebrate digestive system , 1989 .

[31]  A. Thorburn,et al.  Food processing and the glycemic index. , 1985, The American journal of clinical nutrition.

[32]  A. Sclafani,et al.  The effects of ileal transposition on food intake and body weight loss in VMH-obese rats. , 1982, The American journal of clinical nutrition.

[33]  T. Wolever,et al.  Rate of digestion of foods and postprandial glycaemia in normal and diabetic subjects. , 1980, British medical journal.

[34]  B. Grabner,et al.  Jejunoileal Bypass Long‐term Results , 1980, Annals of surgery.

[35]  I. Deschamps,et al.  Effects of Diet on Insulin and Gastric Inhibitory Polypeptide Levels in Obese Children , 1980, Pediatric Research.

[36]  L. F. Burroughs,et al.  DEPLETION AND DISRUPTION OF DIETARY FIBRE EFFECTS ON SATIETY, PLASMA-GLUCOSE, AND SERUM-INSULIN , 1977, The Lancet.

[37]  K. Wynne,et al.  Attenuated peptide YY release in obese subjects is associated with reduced satiety. , 2006, Endocrinology.

[38]  T. Kieffer,et al.  The multifaceted potential of glucagon-like peptide-1 as a therapeutic agent. , 2002, Minerva endocrinologica.

[39]  M. L. Robertson,et al.  Evolutionary perspectives on human nutrition: The influence of brain and body size on diet and metabolism , 1994, American journal of human biology : the official journal of the Human Biology Council.

[40]  J. Holst,et al.  Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus. , 1993, The Journal of clinical investigation.