Roux‐en‐Y gastric bypass compared with equivalent diet restriction: Mechanistic insights into diabetes remission

To investigate the physiological mechanisms leading to rapid improvement in diabetes after Roux‐en‐Y gastric bypass (RYGB) and specifically the contribution of the concurrent peri‐operative dietary restrictions, which may also alter glucose metabolism.

[1]  L. Groop,et al.  Roux-en-Y gastric bypass versus calorie restriction: support for surgery per se as the direct contributor to altered responses of insulin and incretins to a mixed meal. , 2017, Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery.

[2]  V. Kristiansen,et al.  Peptide YY and glucagon-like peptide-1 contribute to decreased food intake after Roux-en-Y gastric bypass surgery , 2016, International Journal of Obesity.

[3]  Benjamin Aribisala,et al.  Very Low-Calorie Diet and 6 Months of Weight Stability in Type 2 Diabetes: Pathophysiological Changes in Responders and Nonresponders , 2016, Diabetes Care.

[4]  C. Cobelli,et al.  Six and 12 Weeks of Caloric Restriction Increases β Cell Function and Lowers Fasting and Postprandial Glucose Concentrations in People with Type 2 Diabetes. , 2015, The Journal of nutrition.

[5]  Reneé H Moore,et al.  GLP-1 Plays a Limited Role in Improved Glycemia Shortly After Roux-en-Y Gastric Bypass: A Comparison With Intensive Lifestyle Modification , 2014, Diabetes.

[6]  T. Sweeney,et al.  Metabolic surgery: action via hormonal milieu changes, changes in bile acids or gut microbiota? A summary of the literature. , 2014, Best practice & research. Clinical gastroenterology.

[7]  C. Bouchard,et al.  Association of bariatric surgery with long-term remission of type 2 diabetes and with microvascular and macrovascular complications. , 2014, JAMA.

[8]  H. Pijl,et al.  Calorie Restriction is a Major Determinant of the Short‐Term Metabolic Effects of Gastric Bypass Surgery in Obese Type 2 Diabetic Patients , 2014, Clinical endocrinology.

[9]  D. Drucker,et al.  Effects of Roux-en-Y gastric bypass on energy and glucose homeostasis are preserved in two mouse models of functional glucagon-like peptide-1 deficiency. , 2014, Molecular metabolism.

[10]  N. Stylopoulos,et al.  GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents. , 2014, American journal of physiology. Regulatory, integrative and comparative physiology.

[11]  J. Holst,et al.  Exaggerated Glucagon-Like Peptide 1 Response Is Important for Improved β-Cell Function and Glucose Tolerance After Roux-en-Y Gastric Bypass in Patients With Type 2 Diabetes , 2013, Diabetes.

[12]  M. Bessler,et al.  Very Low–Calorie Diet Mimics the Early Beneficial Effect of Roux-en-Y Gastric Bypass on Insulin Sensitivity and β-Cell Function in Type 2 Diabetic Patients , 2013, Diabetes.

[13]  E. Livingston,et al.  Rapid Improvement in Diabetes After Gastric Bypass Surgery , 2013, Diabetes Care.

[14]  A. Lacy,et al.  GLP-1 Action and Glucose Tolerance in Subjects With Remission of Type 2 Diabetes After Gastric Bypass Surgery , 2013, Diabetes Care.

[15]  J. Holst,et al.  Mechanisms for the antihyperglycemic effect of sitagliptin in patients with type 2 diabetes. , 2012, The Journal of clinical endocrinology and metabolism.

[16]  J. Holst,et al.  Mechanisms of improved glycaemic control after Roux-en-Y gastric bypass , 2012, Diabetologia.

[17]  P. Pasqualetti,et al.  Very-low-calorie diet: a quick therapeutic tool to improve β cell function in morbidly obese patients with type 2 diabetes. , 2012, The American journal of clinical nutrition.

[18]  J. Holst,et al.  Changes in Gastrointestinal Hormone Responses, Insulin Sensitivity, and Beta-Cell Function Within 2 Weeks After Gastric Bypass in Non-diabetic Subjects , 2012, Obesity Surgery.

[19]  S. Burgess,et al.  Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease. , 2011, Cell metabolism.

[20]  M. Bessler,et al.  Comparison of Glucostatic Parameters After Hypocaloric Diet or Bariatric Surgery and Equivalent Weight Loss , 2011, Obesity.

[21]  S. Ikramuddin,et al.  Changes in gastrointestinal hormones and leptin after Roux-en-Y gastric bypass surgery. , 2011, JPEN. Journal of parenteral and enteral nutrition.

[22]  N. Abumrad,et al.  The Importance of Caloric Restriction in the Early Improvements in Insulin Sensitivity After Roux-en-Y Gastric Bypass Surgery , 2010, Diabetes Care.

[23]  M. Schambelan,et al.  Improvement in Peripheral Glucose Uptake After Gastric Bypass Surgery Is Observed Only After Substantial Weight Loss Has Occurred and Correlates with the Magnitude of Weight Lost , 2009, Journal of Gastrointestinal Surgery.

[24]  D. Cummings Endocrine mechanisms mediating remission of diabetes after gastric bypass surgery , 2009, International Journal of Obesity.

[25]  J. Teixeira,et al.  Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with type 2 diabetes. , 2008, The Journal of clinical endocrinology and metabolism.

[26]  S. Bloom,et al.  Gut Hormones as Mediators of Appetite and Weight Loss After Roux-en-Y Gastric Bypass , 2007, Annals of surgery.

[27]  D. Cummings,et al.  Role of the bypassed proximal intestine in the anti-diabetic effects of bariatric surgery. , 2007, Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery.

[28]  E. Ferrannini,et al.  Effect of Pioglitazone on the Metabolic and Hormonal Response to a Mixed Meal in Type II Diabetes , 2007, Clinical pharmacology and therapeutics.

[29]  S. L. Owens,et al.  Application of stable isotopes and mass isotopomer distribution analysis to the study of intermediary metabolism of nutrients. , 2006, Journal of animal science.

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

[31]  M. Gagner,et al.  The Early Effect of the Roux-en-Y Gastric Bypass on Hormones Involved in Body Weight Regulation and Glucose Metabolism , 2004, Annals of surgery.

[32]  Andrea Mari,et al.  A circulatory model for calculating non-steady-state glucose fluxes. Validation and comparison with compartmental models , 2003, Comput. Methods Programs Biomed..

[33]  Daniel B. Jones,et al.  Clinical predictors of leak after laparoscopic Roux-en-Y gastric bypass for morbid obesity , 2003, Surgical Endoscopy And Other Interventional Techniques.

[34]  Andrea Mari,et al.  Meal and oral glucose tests for assessment of beta -cell function: modeling analysis in normal subjects. , 2002, American journal of physiology. Endocrinology and metabolism.

[35]  R. Bergman,et al.  Accurate Assessment of β-Cell Function: The Hyperbolic Correction , 2002 .

[36]  R. Bergman,et al.  Accurate assessment of beta-cell function: the hyperbolic correction. , 2002, Diabetes.

[37]  Andrea Mari,et al.  A Model-Based Method for Assessing Insulin Sensitivity From the Oral Glucose Tolerance Test , 2001 .

[38]  A Mari,et al.  Dose-response characteristics of insulin action on glucose metabolism: a non-steady-state approach. , 2000, American journal of physiology. Endocrinology and metabolism.

[39]  M. Stumvoll,et al.  Use of the oral glucose tolerance test to assess insulin release and insulin sensitivity. , 2000, Diabetes care.

[40]  M. Matsuda,et al.  Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. , 1999, Diabetes care.

[41]  J. Levy,et al.  Correct Homeostasis Model Assessment (HOMA) Evaluation Uses the Computer Program , 1998, Diabetes Care.

[42]  R. Bergman,et al.  Quantification of the Relationship Between Insulin Sensitivity and β-Cell Function in Human Subjects: Evidence for a Hyperbolic Function , 1993, Diabetes.

[43]  R. Wing,et al.  Relative effects of calorie restriction and weight loss in noninsulin-dependent diabetes mellitus. , 1993, The Journal of clinical endocrinology and metabolism.

[44]  S. Welle,et al.  The safety and efficacy of a controlled low-energy ('very-low-calorie') diet in the treatment of non-insulin-dependent diabetes and obesity. , 1988, Archives of internal medicine.