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Response to M. Deitel
Surgery for Obesity and Related Diseases ] (2015) 00–00
Letter to the editor
Response to M. Deitel To the Editor Dr. M. Deitel speculates about the causes of obesity in type 1 diabetes based almost exclusively on his own theories, as he refers to his own book chapters (edited by Deitel et al.) and papers throughout his communication. Although the causes alluded to may be eventually be shown to be correct, other solid causes described in the literature— the “accelerator hypothesis” among others—should be mentioned [1]. Regarding the comment on the Editorial that followed the Robert et al. paper [2,3], currently there is no question that the Roux-en-Y gastric bypass (RYGB) offers the best risk/benefit profile among all proposed metabolic procedures. I would like to recall for Dr. Deitel some very important issues: 1. There are several weight loss–independent mechanisms related to type 2 diabetes control rather than an explanation based purely on incretin response after a meal [4]. Among them are intestinal sensing mechanism and secondary decreased hepatic insulin resistance [5], increased levels of bile acids and an incretin independent insulin secretion [6], and changes in gut microbiota [7]. Most of those mechanisms decrease hepatic and peripheral insulin resistance, thus leading to a decreased (and not increased) circulating insulin [8]. 2. All those mechanisms were observed experimentally and clinically, mostly after RYGB surgery but also after sleeve gastrectomy (SG) [9–11], and not yet in any version of the mini gastric bypass (MGB) 3. All major randomized controlled trials compared the RYGB, the SG, and even the bileopancreatic diversion– Scopinaro technique to the best medical treatment [12– 16]; there is scarce information comparing any version of the MGB to the well-known traditional techniques and no comparison to any form of medical treatment. Furthermore, the RYGB risk/benefit profile was the best among the operations and outperformed the medical arm in all trials.
4. All case series of any modality of 1 anastomosis gastric bypass (or MGB—there is still some controversy among the names [17]) may be biased in selection of patients. In Lee et al.’s [18] comparison study of the anastomosis duodenal bypass with SG, the authors reported that the single anastomosis operation was longer than the RYGB. Is it really a simple operation? Is the proposed single anastomosis duodenal ileostomy with sleeve gastrectomy [19]—what Dr. Deitel calls “the Spanish version,” which had a considerable number of patients with severe postoperative malnutrition that required revision to treat it—a safe procedure? Can we just name it a bileopancreatic diversion, in theory easier for the surgeon but potentially subjecting patients to a mid- to long-term nutritional burden? Finally, I repeat my statement from the Editorial: so far, RYGB seems to be the best option for medically uncontrolled type 2 diabetes. MGB and its variants have to undergo randomized controlled trials to gauge their real benefit compared with the best medical treatment or any other standard operation. Most importantly, the RYGB and short-, mid-, and long-term complications need to be reported. Ricardo Cohen, M.D. References [1] Kibirige M, Metcalf B, Renuka R, Wilkin TJ. Testing the accelerator hypothesis: the relationship between body mass and age at diagnosis of type 1 diabetes. Diabetes Care 2003;26(10):2865–70. [2] Robert M, Belanger P, Hould FS, Marceau S, Tchernof A, Biertho L. Should metabolic surgery be offered in morbidly obese patients with type I diabetes? Surg Obes Relat Dis 2015;11(4):798–805. [3] Cohen R. Comment on: Should metabolic surgery be offered in morbidly obese patients with type I diabetes? Surg Obes Relat Dis 2015;11(4):805–7. [4] Jiménez A, Casamitjana R, Viaplana-Masclans J, Lacy A, Vidal J. GLP-1 action and glucose tolerance in subjects with remission of type 2 diabetes after gastric bypass surgery. Diabetes Care 2013;36 (7):2062–9.
http://dx.doi.org/10.1016/j.soard.2015.12.008 1550-7289/r 2015 American Society for Metabolic and Bariatric Surgery. All rights reserved.
2
R. Cohen / Surgery for Obesity and Related Diseases ] (2015) 00–00
[5] Breen DM, Rasmussen BA, Kokorovic A, Wang R, Cheung GW, Lam TK. Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes. Nat Med 2012;18(6):950–5. [6] Seeley RJ, Chambers AP, Sandoval DA. The role of gut adaptation in the potent effects of multiple bariatric surgeries on obesity and diabetes. Cell Metab 2015;21(3):369–78. [7] Khan MT, Nieuwdorp M, Bäckhed F. Microbial modulation of insulin sensitivity. Cell Metab 2014;20(5):753–60. [8] Pories WJ, Dohm GL. Diabetes: have we got it all wrong? Hyperinsulinism as the culprit: surgery provides the evidence. Diabetes Care 2012;35(12):2438–42. [9] Nannipieri M, Baldi S, Mari A, et al. Roux-en-Y gastric bypass and sleeve gastrectomy: mechanisms of diabetes remission and role of gut hormones. J Clin Endocrinol Metab 2013;98(11):4391–9. [10] Hansen EN, Tamboli RA, Isbell JM, et al. Role of the foregut in the early improvement in glucose tolerance and insulin sensitivity following Roux-en-Y gastric bypass surgery. Am J Physiol Gastrointest Liver Physiol 2011;300(5):G795–802. [11] Ryan KK, Tremaroli V, Clemmensen C, et al. FXR is a molecular target for the effects of vertical sleeve gastrectomy. Nature 2014;509 (7499):183–8. [12] Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012;366(17):1567–76.
[13] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes — 3-year outcomes. N Engl J Med 2014;370(21):2002–13. [14] Ikramuddin S, Korner J, Lee WJ, et al. Roux-en-Y gastric bypass vs intensive medical management for the control of type 2 diabetes, hypertension, and hyperlipidemia: the Diabetes Surgery Study randomized clinical trial. JAMA 2013;309(21):2240–9. [15] Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med 2012;366(17):1577–85. [16] Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric-metabolic surgery versus conventional medical treatment in obese patients with type 2 diabetes: 5 year follow-up of an open-label, single-centre, randomised controlle trial. Lancet 2015;386(9997):964–73. [17] Carbajo MA, Luque-de-León E. Mini-gastric bypass/one-anastomosis gastric bypass—standardizing the name. Obes Surg 2015;25(5):858–9. [18] Lee WJ, Lee KT, Kasama K, et al. Laparoscopic single-anastomosis duodenal–jejunal bypass with sleeve gastrectomy (SADJB-SG): short-term result and comparison with gastric bypass. Obes Surg 2014;24(1):109–13. [19] Sánchez-Pernaute A, Rubio MÁ, Cabrerizo L, Ramos-Levi A, PérezAguirre E, Torres A. Single-anastomosis duodenoileal bypass with sleeve gastrectomy (SADI-S) for obese diabetic patients. Surg Obes Relat Dis 2015;11(5):1–7.
http://dx.doi.org/10.1016/j.soard.2015.12.008
Letter to the editor
Response to M. Deitel To the Editor Dr. M. Deitel speculates about the causes of obesity in type 1 diabetes based almost exclusively on his own theories, as he refers to his own book chapters (edited by Deitel et al.) and papers throughout his communication. Although the causes alluded to may be eventually be shown to be correct, other solid causes described in the literature— the “accelerator hypothesis” among others—should be mentioned [1]. Regarding the comment on the Editorial that followed the Robert et al. paper [2,3], currently there is no question that the Roux-en-Y gastric bypass (RYGB) offers the best risk/benefit profile among all proposed metabolic procedures. I would like to recall for Dr. Deitel some very important issues: 1. There are several weight loss–independent mechanisms related to type 2 diabetes control rather than an explanation based purely on incretin response after a meal [4]. Among them are intestinal sensing mechanism and secondary decreased hepatic insulin resistance [5], increased levels of bile acids and an incretin independent insulin secretion [6], and changes in gut microbiota [7]. Most of those mechanisms decrease hepatic and peripheral insulin resistance, thus leading to a decreased (and not increased) circulating insulin [8]. 2. All those mechanisms were observed experimentally and clinically, mostly after RYGB surgery but also after sleeve gastrectomy (SG) [9–11], and not yet in any version of the mini gastric bypass (MGB) 3. All major randomized controlled trials compared the RYGB, the SG, and even the bileopancreatic diversion– Scopinaro technique to the best medical treatment [12– 16]; there is scarce information comparing any version of the MGB to the well-known traditional techniques and no comparison to any form of medical treatment. Furthermore, the RYGB risk/benefit profile was the best among the operations and outperformed the medical arm in all trials.
4. All case series of any modality of 1 anastomosis gastric bypass (or MGB—there is still some controversy among the names [17]) may be biased in selection of patients. In Lee et al.’s [18] comparison study of the anastomosis duodenal bypass with SG, the authors reported that the single anastomosis operation was longer than the RYGB. Is it really a simple operation? Is the proposed single anastomosis duodenal ileostomy with sleeve gastrectomy [19]—what Dr. Deitel calls “the Spanish version,” which had a considerable number of patients with severe postoperative malnutrition that required revision to treat it—a safe procedure? Can we just name it a bileopancreatic diversion, in theory easier for the surgeon but potentially subjecting patients to a mid- to long-term nutritional burden? Finally, I repeat my statement from the Editorial: so far, RYGB seems to be the best option for medically uncontrolled type 2 diabetes. MGB and its variants have to undergo randomized controlled trials to gauge their real benefit compared with the best medical treatment or any other standard operation. Most importantly, the RYGB and short-, mid-, and long-term complications need to be reported. Ricardo Cohen, M.D. References [1] Kibirige M, Metcalf B, Renuka R, Wilkin TJ. Testing the accelerator hypothesis: the relationship between body mass and age at diagnosis of type 1 diabetes. Diabetes Care 2003;26(10):2865–70. [2] Robert M, Belanger P, Hould FS, Marceau S, Tchernof A, Biertho L. Should metabolic surgery be offered in morbidly obese patients with type I diabetes? Surg Obes Relat Dis 2015;11(4):798–805. [3] Cohen R. Comment on: Should metabolic surgery be offered in morbidly obese patients with type I diabetes? Surg Obes Relat Dis 2015;11(4):805–7. [4] Jiménez A, Casamitjana R, Viaplana-Masclans J, Lacy A, Vidal J. GLP-1 action and glucose tolerance in subjects with remission of type 2 diabetes after gastric bypass surgery. Diabetes Care 2013;36 (7):2062–9.
http://dx.doi.org/10.1016/j.soard.2015.12.008 1550-7289/r 2015 American Society for Metabolic and Bariatric Surgery. All rights reserved.
2
R. Cohen / Surgery for Obesity and Related Diseases ] (2015) 00–00
[5] Breen DM, Rasmussen BA, Kokorovic A, Wang R, Cheung GW, Lam TK. Jejunal nutrient sensing is required for duodenal-jejunal bypass surgery to rapidly lower glucose concentrations in uncontrolled diabetes. Nat Med 2012;18(6):950–5. [6] Seeley RJ, Chambers AP, Sandoval DA. The role of gut adaptation in the potent effects of multiple bariatric surgeries on obesity and diabetes. Cell Metab 2015;21(3):369–78. [7] Khan MT, Nieuwdorp M, Bäckhed F. Microbial modulation of insulin sensitivity. Cell Metab 2014;20(5):753–60. [8] Pories WJ, Dohm GL. Diabetes: have we got it all wrong? Hyperinsulinism as the culprit: surgery provides the evidence. Diabetes Care 2012;35(12):2438–42. [9] Nannipieri M, Baldi S, Mari A, et al. Roux-en-Y gastric bypass and sleeve gastrectomy: mechanisms of diabetes remission and role of gut hormones. J Clin Endocrinol Metab 2013;98(11):4391–9. [10] Hansen EN, Tamboli RA, Isbell JM, et al. Role of the foregut in the early improvement in glucose tolerance and insulin sensitivity following Roux-en-Y gastric bypass surgery. Am J Physiol Gastrointest Liver Physiol 2011;300(5):G795–802. [11] Ryan KK, Tremaroli V, Clemmensen C, et al. FXR is a molecular target for the effects of vertical sleeve gastrectomy. Nature 2014;509 (7499):183–8. [12] Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012;366(17):1567–76.
[13] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes — 3-year outcomes. N Engl J Med 2014;370(21):2002–13. [14] Ikramuddin S, Korner J, Lee WJ, et al. Roux-en-Y gastric bypass vs intensive medical management for the control of type 2 diabetes, hypertension, and hyperlipidemia: the Diabetes Surgery Study randomized clinical trial. JAMA 2013;309(21):2240–9. [15] Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med 2012;366(17):1577–85. [16] Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric-metabolic surgery versus conventional medical treatment in obese patients with type 2 diabetes: 5 year follow-up of an open-label, single-centre, randomised controlle trial. Lancet 2015;386(9997):964–73. [17] Carbajo MA, Luque-de-León E. Mini-gastric bypass/one-anastomosis gastric bypass—standardizing the name. Obes Surg 2015;25(5):858–9. [18] Lee WJ, Lee KT, Kasama K, et al. Laparoscopic single-anastomosis duodenal–jejunal bypass with sleeve gastrectomy (SADJB-SG): short-term result and comparison with gastric bypass. Obes Surg 2014;24(1):109–13. [19] Sánchez-Pernaute A, Rubio MÁ, Cabrerizo L, Ramos-Levi A, PérezAguirre E, Torres A. Single-anastomosis duodenoileal bypass with sleeve gastrectomy (SADI-S) for obese diabetic patients. Surg Obes Relat Dis 2015;11(5):1–7.
http://dx.doi.org/10.1016/j.soard.2015.12.008