Metabolic syndrome is strictly associated with morbid obesity and leads to an increased risk of cardiovascular diseases and related mortality. Bariatric surgery is considered an effective option for the management of these patients. We searched MEDLINE, Current Contents, and the Cochrane Library for papers published on bariatric surgery outcomes in English from 1 January 1990 to 20 July 2012. We reported the effect of gastrointestinal manipulation on metabolic syndrome after bariatric surgery. Bariatric surgery determines an important resolution rate of major obesity-related comorbidities. Roux-en-Y gastric bypass and biliopancreatic diversion appear to be more effective than adjustable gastric banding in terms of weight loss and comorbidities resolution. However, the results obtained in terms of weight loss and resolution of comorbidities after a “new bariatric procedure” (sleeve gastrectomy) encouraged and stimulated the diffusion of this operation. 1. Introduction In 2008 there were worldwide an estimated 1.5 billion adults overweight and 500 million obese. More than 40 million children are estimated to be overweight. Obesity rates have more than doubled since 1980, with 1 in 10 of the world’s adult western population now obese. Morbid obesity (BMI > 35) is responsible for more than 2.5 million deaths per year worldwide [1], and it has been estimated that life expectancy of a 25-year-old morbidly obese man is 12 years lower because of this condition. In morbidly obese patients, metabolic syndrome (MetS) is a constellation of metabolic abnormalities, including type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia, and ovarian polycystic syndrome, that lead to an increased risk of cardiovascular diseases and related mortality [2]. The physiopathology of MetS is not completely known, but there is an intertwined link between obesity (BMI > 30), insulin resistance, and the MetS, which leads to a vicious cycle of metabolic stress with relevant clinical pattern [3]. Moreover, it has long been assumed that the presence of MetS is a risk factor for adverse outcomes in patients undergoing bariatric/metabolic surgery. In fact, in obese patients with MetS, central and visceral adiposity and hepatomegaly make bariatric surgery more technically challenging. Furthermore, in these patients MetS leads to a heightened state of systematic inflammation, with consequent lower ability to face the stress of bariatric surgery and limitations of body’s response to complications [4]. We describe the effects of the main laparoscopic bariatric/metabolic procedures on MetS
References
[1]
World Health Organization, World Health Report, [WWW document], 2002, http://www.who.int/whr/2002/en/whr02_en.pdf.
[2]
S. M. Grundy, H. B. Brewer Jr., J. I. Cleeman, S. C. Smith, and C. Lenfant, “Definition of metabolic syndrome: report of the national heart, lung, and blood institute/American heart association conference on scientific issues related to definition,” Circulation, vol. 109, no. 3, pp. 433–438, 2004.
[3]
W. B. Inabnet III, D. A. Winegar, B. Sherif, and M. G. Sarr, “Early outcomes of bariatric surgery in patients with metabolic syndrome: an analysis of the bariatric outcomes longitudinal database,” Journal of the American College of Surgeons, vol. 214, no. 4, pp. 550–556, 2012.
[4]
D. W. Richardson, M. E. Mason, and A. I. Vinik, “Update: metabolic and cardiovascular consequences of bariatric surgery,” Endocrinology and Metabolism Clinics of North America, vol. 40, no. 1, pp. 81–96, 2011.
[5]
J. A. Tice, L. Karliner, J. Walsh, A. J. Petersen, and M. D. Feldman, “Gastric banding or bypass? A systematic review comparing the two most popular bariatric procedures,” American Journal of Medicine, vol. 121, no. 10, pp. 885–893, 2008.
[6]
G. R. Silberhumer, K. Miller, A. Pump et al., “Long-term results after laparoscopic adjustable gastric banding in adolescent patients: follow-up of the Austrian experience,” Surgical Endoscopy, vol. 25, no. 9, pp. 2993–2999, 2011.
[7]
J. B. Dixon, P. E. O'Brien, J. Playfair et al., “Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial,” The Journal of the American Medical Association, vol. 299, no. 3, pp. 316–323, 2008.
[8]
K. Wickremesekera, G. Miller, T. D. Naotunne, G. Knowles, and R. S. Stubbs, “Loss of insulin resistance after Roux-en-Y gastric bypass surgery: a time course study,” Obesity Surgery, vol. 15, no. 4, pp. 474–481, 2005.
[9]
G. H. Ballantyne, D. Farkas, S. Laker, and A. Wasielewski, “Short-term changes in insulin resistance following weight loss surgery for morbid obesity: laparoscopic adjustable gastric banding versus laparoscopic Roux-en-Y gastric bypass,” Obesity Surgery, vol. 16, no. 9, pp. 1189–1197, 2006.
[10]
P. C. Sala, R. S. Torrinhas, S. B. Heymsfield, and D. L. Waitzberg, “Type 2 diabetes mellitus: a possible surgically reversible intestinal dysfunction,” Obesity Surgery, vol. 22, no. 1, pp. 167–176, 2012.
[11]
L. Sj?str?m, A. K. Lindroos, M. Peltonen et al., “Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery,” The New England Journal of Medicine, vol. 351, no. 26, pp. 2683–2693, 2004.
[12]
P. R. Schauer, B. Burguera, S. Ikramuddin et al., “Effect of laparoscopic Roux-En Y gastric bypass on type 2 diabetes mellitus,” Annals of Surgery, vol. 238, no. 4, pp. 467–485, 2003.
[13]
T. C. Hall, M. G. C. Pellen, P. C. Sedman, and P. K. Jain, “Preoperative factors predicting remission of type 2 diabetes mellitus after Roux-en-Y gastric bypass surgery for obesity,” Obesity Surgery, vol. 20, no. 9, pp. 1245–1250, 2010.
[14]
J. B. Dixon and P. E. O'Brien, “Lipid profile in the severely obese: changes with weight loss after lap-band surgery,” Obesity Research, vol. 10, no. 9, pp. 903–910, 2002.
[15]
A. Obeid, J. Long, M. Kakade, R. H. Clements, R. Stahl, and J. Grams, “Laparoscopic Roux-en-Y gastric bypass: long term clinical outcomes,” Surgical Endoscopy. In press.
[16]
N. Scopinaro, G. M. Marinari, G. B. Camerini, F. S. Papadia, and G. F. Adami, “Specific effects of biliopancreatic diversion on the major components of metabolic syndrome: a long-term follow-up study,” Diabetes Care, vol. 28, no. 10, pp. 2406–2411, 2005.
[17]
G. F. Adami, R. Cordera, G. Camerini, G. M. Marinari, and N. Scopinaro, “Recovery of insulin sensitivity in obese patients at short term after biliopancreatic diversion,” Journal of Surgical Research, vol. 113, no. 2, pp. 217–221, 2003.
[18]
D. L. Sarson, N. Scopinaro, and S. R. Bloom, “Gut hormone changes after jejunoileal (JIB) or biliopancreatic (BPB) bypass surgery for morbid obesity,” International Journal of Obesity, vol. 5, no. 5, pp. 471–480, 1981.
[19]
G. Silecchia, C. Boru, A. Pecchia et al., “Effectiveness of laparoscopic sleeve gastrectomy (first stage of biliopancreatic diversion with duodenal switch) on co-morbidities in super-obese high-risk patients,” Obesity Surgery, vol. 16, no. 9, pp. 1138–1144, 2006.
[20]
M. Rizzello, F. Abbatini, G. Casella et al., “Early postoperative insulin-resistance changes after sleeve gastrectomy,” Obesity Surgery, vol. 20, no. 1, pp. 50–55, 2010.
[21]
F. Abbatini, M. Rizzello, G. Casella et al., “Long-term effects of laparoscopic sleeve gastrectomy, gastric bypass, and adjustable gastric banding on type 2 diabetes,” Surgical Endoscopy and Other Interventional Techniques, vol. 24, no. 5, pp. 1005–1010, 2010.
[22]
A. L. DePaula, A. L. V. Macedo, N. Rassi et al., “Laparoscopic treatment of type 2 diabetes mellitus for patients with a body mass index less than 35,” Surgical Endoscopy and Other Interventional Techniques, vol. 22, no. 3, pp. 706–716, 2008.
[23]
G. Schernthaner and J. M. Morton, “Bariatric surgery in patients with morbid obesity and type 2 diabetes,” Diabetes Care, vol. 31, supplement 2, pp. S297–S302, 2008.
[24]
K. S. Polonsky, B. Gumbiner, D. Ostrega, K. Griver, H. Tager, and R. R. Henry, “Alterations in immunoreactive proinsulin and insulin clearance induced by weight loss in NIDDM,” Diabetes, vol. 43, no. 7, pp. 871–877, 1994.
[25]
B. Gumbiner, E. van Cauter, W. F. Beltz et al., “Abnormalities of insulin pulsatility and glucose oscillations during meals in obese noninsulin-dependent diabetic patients: effects of weight reduction,” Journal of Clinical Endocrinology and Metabolism, vol. 81, no. 6, pp. 2061–2068, 1996.
[26]
F. Rubino, “Is type 2 diabetes an operable intestinal disease? A provocative yet reasonable hypothesis,” Diabetes Care, vol. 31, supplement 2, pp. 290–296, 2008.
[27]
F. Rubino and J. Marescaux, “Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease,” Annals of Surgery, vol. 239, no. 1, pp. 1–11, 2004.
[28]
A. D. Strader, T. R. Clausen, S. Z. Goodin, and D. Wendt, “Ileal interposition improves glucose tolerance in low dose streptozotocin-treated diabetic and euglycemic rats,” Obesity Surgery, vol. 19, no. 1, pp. 96–104, 2009.
[29]
F. Rubino, A. Forgione, D. E. Cummings et al., “The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes,” Annals of Surgery, vol. 244, no. 5, pp. 741–749, 2006.
[30]
G. Silecchia, D. Capoccia, M. C. Ribaudo et al., “Improvement of insulin sensitivity and diabetes in patients after laparoscopic bariatric surgery2006,” Obesity Surgery, vol. 16, no. 8, article 972.
[31]
J. Vidal, A. Ibarzabal, F. Romero et al., “Type 2 diabetes mellitus and the metabolic syndrome following sleeve gastrectomy in severely obese subjects,” Obesity Surgery, vol. 18, no. 9, pp. 1077–1082, 2008.
[32]
M. Bose, B. Oliván, J. Teixeira, F. X. Pi-Sunyer, and B. Laferrère, “Do incretins play a role in the remission of type 2 diabetes after gastric bypass surgery: what are the evidence?” Obesity Surgery, vol. 19, no. 2, pp. 217–229, 2009.
[33]
S. N. Karamanakos, K. Vagenas, F. Kalfarentzos, and T. K. Alexandrides, “Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: a prospective, double blind study,” Annals of surgery, vol. 247, no. 3, pp. 401–407, 2008.
[34]
R. Peterli, B. W?lnerhanssen, T. Peters et al., “Improvement in glucose metabolism after bariatric surgery: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: a prospective randomized trial,” Annals of Surgery, vol. 250, no. 2, pp. 234–241, 2009.
[35]
D. Pacheco, D. A. de Luis, A. Romero et al., “The effects of duodenal-jejunal exclusion on hormonal regulation of glucose metabolism in Goto-Kakizaki rats,” American Journal of Surgery, vol. 194, no. 2, pp. 221–224, 2007.
[36]
A. Patriti, E. Facchiano, C. Annetti et al., “Early improvement of glucose tolerance after ileal transposition in a non-obese type 2 diabetes rat model,” Obesity Surgery, vol. 15, no. 9, pp. 1258–1264, 2005.
[37]
A. C. Ramos, M. P. Galv?o Neto, Y. M. de Souza et al., “Laparoscopic duodenal-jejunal exclusion in the treatment of type 2 diabetes mellitus in patients with BMI < 30?kg/m2 (LBMI),” Obesity Surgery, vol. 19, no. 3, pp. 307–312, 2009.
[38]
H. Buchwald, Y. Avidor, E. Braunwald et al., “Bariatric surgery: a systematic review and meta-analysis,” The Journal of the American Medical Association, vol. 292, no. 14, pp. 1724–1737, 2004.
[39]
H. Buchwald, R. Estok, K. Fahrbach et al., “Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis,” American Journal of Medicine, vol. 122, no. 3, pp. 248.e5–256.e5, 2009.
[40]
V. G. Athyros, K. Tziomalos, A. Karagiannis, and D. P. Mikhailidis, “Cardiovascular benefits of bariatric surgery in morbidly obese patients,” Obesity Reviews, vol. 12, no. 7, pp. 515–524, 2011.