ABSTRACT

The effective treatment of obesity is challenging. This in part reflects the complexity of the underlying disease process. However, there are a growing number of effective surgical, endoscopic, and pharmacologic treatments which are available. Although there has long been a preference on lifestyle modification such as diet and exercise, there is a relative paucity of evidence to support these interventions as effective long-term treatments for obesity, in producing sustained weight loss and resultant improvements in obesity related disease and mortality. Conversely, bariatric procedures which include sleeve gastrectomy, roux en Y gastric bypass, single anastomosis gastric bypass, biliopancreatic diversion, and several less frequently performed operations have been shown to produce substantial and durable weight loss with significant improvements in obesity related disease, quality of life, and mortality. The mechanisms by which these operations work vary depending on the procedure however they primarily act via alterations in the gut-brain axis and alterations in neurohormonal signaling. These changes produce sustained changes in appetite and hunger and unlike weight loss mediated by diet are not followed by a rebound weight regain in the long term. In addition, there appear to be modifications in bile acid metabolism and the gut microbiome which also play a contributory role in weight loss following bariatric surgery.

The criteria for consideration of bariatric surgery have recently been updated to reflect advances in knowledge, surgical technique, and safety. According to the 2022 guidelines produced by the International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO), people with a BMI >35kg/m² should be recommended surgery and those with BMI 30-34.9kg/m² with metabolic disease should be considered. It is important to involve the multidisciplinary team in determining suitability for surgery as well as for long-term follow up (1). The multidisciplinary team typically includes a dietician, psychologist, physician, and surgeon. The decision on which procedure should be used is based on patient or surgeon preference, availability of appropriate aftercare and the patient’s tolerance of risk and permanent anatomical change. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

BACKGROUND

The hallmark of an effective treatment of obesity is not one which can produce clinically weight loss, rather one which can produce weight loss which is sustained in the long term such that there is an improvement in obesity related disease and mortality. Although diet and lifestyle modification has long been the cornerstone of many obesity treatment programs, the primary concern with such approaches including very low energy diets (VLED) is the durability of weight loss. Randomized controlled trials have shown that weight loss of up to 15% is possible in people living with obesity however less than 10% will maintain this over one year and the majority will return to their pre-diet weight within 3-5 years (2). Conversely, bariatric surgery has been demonstrated to produce weight loss of 20-30% which critically is not only sustained in the long-term but has the effect of modifying the underlying disease process and resetting of the homeostatic weight ‘set point’, primarily through neurohormonal changes (3, 4).

The concept of the set point suggests that in the majority of adults, there is a pre-determined inherent weight around which each individual will maintain their weight over the long-term with a gradual increase seen over time. Following a period of volitional weight loss with dietary changes, there is a decrease in the overall weight followed by several homeostatic adaptations which see a return to the original baseline weight. Following bariatric surgery, irrespective of the procedure performed, there tends to be an initial period of rapid weight loss for the first 18 months followed by a period of weight stability and a subsequent very gradual weight regain. In spite of the recognized weight regain, what is critical is that overall, following surgery, there is a new, lower set point with a similar weight gain trajectory as to what is seen in the general population.

It was initially felt that bariatric procedures could be classified according to the mechanism by which they were thought to act, resulting in the description of ‘restrictive’ and ‘malabsorptive’ procedures however subsequent mechanistic studies have demonstrated this to be incorrect as they were recognized to act via alterations in neurohormonal signaling, bile acid metabolism, and changes in the microbiome (5).

The longest-term data establishing the role of bariatric surgery as a treatment for obesity compared to traditional lifestyle interventions comes from the landmark Swedish Obese Subjects (SOS) study (3). With more than 25 years of follow up, this case-control series demonstrated that irrespective of the procedure performed, bariatric surgery produces sustained weight loss which is maintained long term and supports a reduction in all-cause mortality due to cardiovascular causes and cancer compared to matched controls receiving standard care at the time (6). Critically, in addition to producing sustained weight loss, evidence from randomized controlled trials (RCTs) have consistently supported the efficacy of bariatric surgery in the treatment of obesity related disease, specifically type 2 diabetes mellitus (T2DM) compared to medical treatment (7-18).

In light of improvements in glycemic control and even remission of diabetes in a subset of people with obesity, bariatric surgery forms a central element in the treatment algorithm as endorsed by the American Diabetes Association (ADA) and International Diabetes Federation (IDF) for those with obesity and T2DM. Early views of gastrointestinal surgery as a means of permanently curing diabetes have been replaced by a more realistic view that it is more likely a means of inducing remission and improving long term glycemic control. Longer-term data from studies has now demonstrated that one in four people who initially go into remission will experience a relapse of T2DM (7). Despite this, it is essential to recognize that although some of the metabolic improvements associated with surgery dissipate with time, glycemic control is still very good compared to those treated with medication alone. As demonstrated by the UK Prospective Diabetes Study (UKPDS), there is a legacy effect of even a short period of improved glycemic control on the development of diabetes-related complications, cardiovascular endpoints and mortality (19). Thus, even individuals who do not meet the ADA criteria for diabetes remission, these improvements in glycemic control should not be dismissed as they may have important implications for morbidity and mortality.

A HISTORICAL PERSPECTIVE OF BARIATRIC SURGERY

Surgical procedures involving the upper gastrointestinal tract have long been recognized to result in substantial and sustained reductions in weight, albeit most often to the detriment of the patient. Although the mechanisms producing this weight loss were at the time very poorly understood, it became apparent that this effect could be used within the context of obesity to potentially produce surgically mediated weight loss with an improvement in metabolic disease.

CURRENT METHODS IN BARIATRIC SURGERY

Sleeve Gastrectomy

The sleeve gastrectomy (SG) has become the most commonly performed bariatric procedure worldwide. Although initially conceived as part of the two-stage duodenal switch procedure SG has become a standalone operation having recognized the substantial weight loss it produces as well as improvement in obesity associated disease. SG involves excision of approximately 80% of the stomach by using multiple firings of a linear stapler/cutter to separate a narrow tube or sleeve of the lesser curve of the stomach from the greater curve. The initial firing starts approximately 4-7cm proximal to the pylorus which is preserved to maintain gastric emptying. A bougie (usually >32Fr) is placed in the lesser curve segment during the resection to maintain adequate lumen size. Although there is variability in the precise size, a 2012 consensus statement recommended the use of a bougie between 32-40Fr (38).

SG is relatively contraindicated in those with significant gastro-esophageal reflux disease (GERD) due to the high risk of worsening of pre-existing reflux and which can be difficult to manage symptomatically and may also play a role in the development of Barrett’s esophagus. Due to this potential risk, it is advised by the International Federation for the Surgery of Obesity (IFSO) that any person undergoing SG have surveillance endoscopy one year postoperatively and then every 2-3 years thereafter (39). Other recognized complications of SG include staple line leak and bleeding in the early postoperative period as well as de novo or worsening of GERD and stricture. As the gastric remnant is removed, SG is not a reversible procedure.

Although initially and incorrectly classified as a procedure that acted via mechanical restriction, mechanistic studies have demonstrated that SG acts by modifying key neurohormones including GLP-1 and PYY which regulate hunger, appetite, and satiety via the gut-brain axis (40). SG is also thought to reduce hunger through resection of the gastric fundus which is the site of ghrelin production (41).

Figure 1.

Sleeve gastrectomy.

Laparoscopic Adjustable Gastric Banding (LAGB)

At one time LAGB was one of the most commonly performed bariatric procedures, however, it is now infrequently performed due to the perceived high complication and re-operation rate as well as the mounting evidence to support that that it does not produce equivalent weight loss to procedures such as SG and RYGB. Although previous studies have demonstrated nearly 50% excess weight loss that can be maintained with >15 year follow up, the major caveat was the requirement for very close follow up with regular band adjustments which was not sustainable in real world practice (42).

In spite of the apparent limitations of the LAGB, the less invasive nature of the operation and potential reversibility of the procedure make it a potential consideration for those who are considered higher risk. Recognized complications of LAGB include port site infection, GERD, pouch dilatation, band slippage and erosion. Studies have suggested that up to 50% of those who have a LAGB will require reoperation or band removal (43).

The exact mechanisms of action of the LAGB are unclear however they are thought to act beyond the pure mechanical effect by involving vagal afferents (44). Vagal stimulation may help regulate food intake by promoting satiety.

Figure 2.

The band consists of a ring of silicone with an inner balloon. The balloon is connected to an access port.

Figure 3.

The LAGB is placed over the cardia of the stomach within 1cm of the esophago-gastric junction.

Roux en Y Gastric Bypass (RYGB)

Roux en Y gastric bypass is now less commonly performed than SG due in part to the technical challenge of forming two anastomoses and previous lack of level one evidence demonstrating its superiority in terms of weight loss or resolution of obesity related disease. The emergence of recent data from several RCTs appears to support that RYGB may produce significantly higher weight loss than SG with greater improvements in obesity related disease including dyslipidemia and gastro-esophageal reflux disease (GERD). Overall, there is good long-term evidence to support the efficacy of RYGB as a safe procedure which provides significant and durable weight loss with a significant improvement in metabolic complications such as T2DM (7, 45). It is also the procedure of choice in those with significant pre-existing GERD and obesity rather than SG (46).

Similar to SG, studies have shown that RYGB produces weight loss through changes in gut hormones, namely GLP-1 and PYY, an effect which is believed to be in part the result of early delivery of nutrient in the terminal ileum and passage of undiluted bile in the bypass and the proximal jejunum (4, 5). These changes appear within days of surgery and as well as producing long-term reductions in weight are also responsible for the weight-loss independent improvements in glucose homeostasis which occur in the immediate postoperative period.

RYGB involves the formation of a small gastric pouch with an excluded gastric remnant. A loop of jejunum is then brought up and anastomosed to the gastric pouch to form the gastro-jejunostomy with the alimentary limb distal to this. Within the alimentary limb, ingested food is excluded from mixing with any digestive enzymes as the proximal jejunum has been bypassed. Approximately 100-120cm distal to the gastro-jejunostomy, a second anastomosis is formed between the biliary limb and the alimentary limb to form the jejuno-jejunostomy. It is only distal to this anastomosis that there is mixing of food and bile.

Although this is overall a very safe procedure, the most potentially serious complication which may arise is bowel obstruction or ischemia secondary to an internal hernia as two mesenteric defects are created during the procedure. Both mesenteric defects are typically closed intraoperatively, however, they may increase in size over time following weight loss and as the fat content of the mesentery decreases. Studies would support the routine closure of mesenteric defects but doing so is associated with an increased risk of complications associated with small bowel obstruction at the jejunojejunostomy (47). Additional complications include the possibility of anastomotic leaks or stricture and staple line bleeding. A small minority of people may also develop chronic abdominal pain which may be challenging to treat. It is also worth noting that due to the anatomical changes produced by RYGB, future procedures such as ERCP may require alternative approaches to accessing the excluded proximal duodenum via the remnant stomach. This may also be of concern in populations where there is concern about gastric cancer as the remnant stomach cannot be assessed by standard esophagogastroduodenoscopy.

Figure 4.

RYGB showing a small gastric pouch, a narrow gastrojejunostomy and exclusion of foods from the duodenum and proximal jejunum.

One Anastomosis Gastric Bypass (OAGB)

The one gastric bypass is increasingly popular as an alternative to the RYGB owing in part to the fact that it produces significant weight loss but requires the formation of only one anastomosis. OAGB involves the formation of a small gastric pouch to which a loop of jejunum is anastomosed to form a gastro-jejunostomy. Unlike the RYGB, there is only one anastomosis and the length of duodenum and proximal jejunum which is bypassed is much longer, typically up to 150cm (48, 49). (figure 5).

The mechanism of action is thought to be very similar to that of RYGB in that it results in changes in gut hormone signaling via bypass of the proximal duodenum and studies to date would suggest that weight loss outcomes as a result are comparable (48). These changes are also responsible for the improvements in glucose homeostasis and resolution or improvement of T2DM.

Given the relative lack of long-term follow up on OAGB, there are concerns regarding the potential implications of chronic bile acid reflux and the possibility of inducing gastric and esophageal malignancy, however, there is no high-quality evidence at present to support these concerns.

Figure 5.

OAGB showing the gastric pouch as a sleeve of lesser curve of stomach and the loop gastrojejunostomy.

Biliopancreatic Diversion / Duodenal Switch (BPD/DS)

Although BPD/DS is not amongst the most commonly performed bariatric procedures, accounting for only ~1% of operations worldwide, it is noteworthy for the amount of weight loss it induces as well as the resultant improvements in metabolic dysfunction. The operation is a two-stage procedure with the initial operation involving the formation of a sleeve gastrectomy with preservation of the pylorus. In the second stage, the duodenum is mobilized and divided at D1 and subsequently anastomosed to the distal ileum. The duoden-ileal anastomosis forms the alimentary limb through which ingested food will pass, without mixing with digestive enzymes. A second anastomosis is then formed between the biliary limb and the distal ileum, approximately 80-100cm proximal to the ileocecal valve. The second anastomosis creates a short common channel for mixing of ingested food and digestive enzymes.

The weight loss and metabolic improvements following BPD/DS are significantly greater than RYGB/OAGB and SG, however, it remains an infrequently performed procedure not only due to the technical challenges but primarily owing to significant long-term complications. As a result of the very short common channel, micronutrient and fat-soluble vitamin deficiencies are expected and long-term supplementation and monitoring is essential. The potential complications resulting from nutrient deficiency can be severe and in cases irreversible, including night blindness and Wernicke’s encephalopathy. Up to 10% will remain deficient despite adherence to dietary and nutritional guidelines and supplementation and will require re-operation (50).

Figure 6.

The DS variant of BPD with a sleeve gastrectomy, retention of the gastric antrum, diversion of food into the mid small gut and diversion of pancreatic and biliary secretions to the distal small gut. Note both limbs are passing behind the transverse colon and a color difference is added to help follow the respective pathways. The common channel is the normal ileum terminating at the ileo-cecal junction.

MECHANISMS OF ACTION IN BARIATRIC SURGERY

Although the development of the set point theory would support that for the majority of adults, there appears to be a pre-determined inherent weight around which most will not significantly deviate from in the long term, there appear to be profound changes following bariatric surgery which contribute to weight loss which is maintained. Irrespective of the procedure performed, people tend to demonstrate a similar weight loss pattern following surgery with an initial period of rapid weight loss for the first 18 months followed by a period of weight stability and a subsequent very gradual weight regain. In spite of the recognized weight regain, what is key is that overall, following surgery, there seems to be a new, lower set point and the adoption of a similar weight gain trajectory as to what is seen in the general population.

Early views of bariatric surgery saw procedures characterized according to the mechanism by which they were thought to act with sleeve gastrectomy (SG) described as a volume reducing surgery, biliopancreatic diversion (BPD) seen as a hypoabsorptive procedure and Roux en Y gastric bypass (RYGB) as both. Subsequent mechanistic and behavioral studies have since produced greater insights in to the mechanisms of weight regulation, alterations in appetite and satiety and neurohormonal changes as well as bile acid metabolism which are now recognized as key regulators resulting in weight loss an improvement in metabolic dysfunction (41, 57, 58).

OUTCOMES AFTER BARIATRIC SURGERY

OTHER HEALTH OUTCOMES AFTER BARIATRIC SURGERY

IMPROVEMENT IN QUALITY OF LIFE (QOL)

Several studies clearly demonstrate major QOL improvements following bariatric procedures (145-149). A large prospective study of QOL after bariatric surgery employed the Medical Outcomes Trust Short Form-36 (SF-36). The SF-36 is a reliable, broadly used instrument that has been validated in people living with obesity. In this study, 459 participants with complex obesity were found to have lower scores compared with a control population for all 8 aspects of QOL measured, particularly the physical health scores. Weight loss provided a dramatic and sustained improvement in all measures of the SF-36. Improvement was greater in those with more preoperative disability; however, the extent of weight loss was not a good predictor of improved QOL. Even for patients who required revisional surgery during the follow-up period, they found a similar improvement in measures of QOL. Similar improvements in QOL have been demonstrated in patients having LAGB for previously failed gastric stapling (150).

IMPROVEMENT IN SURVIVAL

The ultimate test of effectiveness of a treatment is the reduction of mortality. There is a growing body of evidence on long-term mortality of people who have undergone bariatric surgery compared to people with obesity who have not had surgery which shows improved survival. The SOS study demonstrated that over a median follow up period of 24 years that there was a lower risk of mortality in the people who had undergone surgery compared to the matched controls which resulted in a median increase in life expectancy by 2.4 years (6). The risk of death from both cardiovascular risk but also cancer was lower in the patients who had undergone surgery. In spite of these improvements, the group of patients who had undergone surgery still had an 8-year shorter life expectancy relative to the general population with the leading cause of death being cardiovascular disease.

A systematic review and meta-analysis of 16 matched cohort studies and one prospective controlled trial found that there is a median improvement in life expectancy of 6.1 years in patients who had undergone bariatric surgery compared to usual care. Although both participants with and without T2DM demonstrated an increased overall survival, the treatment effect was considerably larger for those with T2DM with an increased life expectancy of 9.3 years compared to the non-surgical group. The number needed to treat to prevent one additional death in 10 years was 8.4 for people with T2DM compared to 29.8 for those without (151).

FUTURE DIRECTIONS COMBINING MEDICATIONS WITH SURGERY

There has long been a focus on comparing outcomes for the treatments of obesity and related diseases, particularly T2DM looking at the use of either surgery or medical therapy. Although studies have consistently demonstrated the efficacy of surgery in achieving long-term reductions in weight and improvements in diabetes, it is clear from our understanding of the disease process itself that obesity is a chronic and progressive disease which will over time require treatment intensification. Looking to the management of other diseases, including cancer, surgery is often viewed as a means of establishing disease control with adjunctive medical therapies to sustain this effect in the long-term (152, 153).

The concept of utilizing medication with bariatric surgery has been demonstrated to be both safe and effective as demonstrated by the STAMPEDE trial in which both RYGB and SG were combined with IMT. Impressive advances in pharmacotherapy initially developed as anti-diabetes medications but equally recognized for its efficacy in producing weight loss in people without diabetes has made the potential for employing multi-modal care even more promising, improving long term disease control and remission.

WHO SHOULD BE CONSIDERED FOR BARIATRIC SURGERY?

For many years, the criteria for bariatric surgery were largely based on the National Institutes of Health (NIH) guidelines issued more than 30 years ago in 1991 (154). These guidelines were highly constrained by BMI cut offs and based on surgical outcomes from the era of open surgery. Having recognized the significant advances in surgery, safety outcomes as well as our greater understanding of the disease process, related disease, and mechanisms of action of surgery, IFSO and ASMBS jointly released updated guidelines in 2022 (1).

Major changes to the previous guidelines include:

• Metabolic and bariatric surgery (MBS) is recommended for individuals with BMI>35kg/m² regardless of the presence of obesity related disease.
• MBS should be considered for individuals with a BMI 30-34.9kg/m² with metabolic disease.
• BMI thresholds should be adjusted in the Asian population such that a BMI>25kg/m² suggests clinical obesity and individuals with a BMI>27.5kg/m² are offered MBS.
• Appropriately selected children and adolescents should be considered for MBS.

NEEDS AND CHALLENGES

Bariatric surgery should be viewed as a process of care that begins with a careful initial clinical evaluation and detailed patient education, continuing beyond the operative procedure through a permanent follow-up. The increasing number of safe and effective bariatric procedures should be seen as part of a growing number of treatments for obesity which may need to be combined in a stepwise and progressive approach to achieve long-term disease control. Improving care for people with obesity undergoing bariatric surgery is an evolving process as our understanding of the disease itself and its implications for people living with obesity deepens. Future areas which remain to be improved include.

• A better understanding of the mechanisms of action of each procedure is required to enable optimum surgery and follow up.
• Accurate and comprehensive data management. Bariatric surgical procedures should be incorporated into national clinical registries to enable objective assessment of the risks and benefits across the community.
• More randomized controlled trials to improve our understanding of the long-term outcomes of different procedures and their implications for control of obesity related co-morbidity
• Improved evidence-based decision-making pathways to help determine who would benefit most from bariatric surgery.
• High quality clinical trials looking at the use of multimodal care, combining bariatric surgery with pharmacotherapy to improve long-term disease remission and control.
• Definition of safe and efficient pathways for assessment, surgery. and post-surgery care.
• Greater focus on understanding the implications of obesity stigma, how it affects patient care and what clinicians can do to address these inequalities.

Bariatric surgery has the potential to be one of the most important and powerful treatment approaches in medicine. High quality clinical care, good science, and comprehensive data management will allow optimal application of this approach to be realized.

REFERENCES

1.

Eisenberg D, Shikora SA, Aarts E, Aminian A, Angrisani L, Cohen RV, et al. 2022 American Society of Metabolic and Bariatric Surgery (ASMBS) and International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) Indications for Metabolic and Bariatric Surgery. Obes Surg. 2023;33(1):3-14. [PMC free article: PMC9834364] [PubMed: 36336720]

2.

Lean MEJ, Leslie WS, Barnes AC, Brosnahan N, Thom G, McCombie L, et al. Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year results of the DiRECT open-label, cluster-randomised trial. Lancet Diabetes Endocrinol. 2019;7(5):344-55. [PubMed: 30852132]

3.

Sjöström L, Narbro K, Sjöström CD, Karason K, Larsson B, Wedel H, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741-52. [PubMed: 17715408]

4.

Pournaras DJ, Aasheim ET, Bueter M, Ahmed AR, Welbourn R, Olbers T, et al. Effect of bypassing the proximal gut on gut hormones involved with glycemic control and weight loss. Surg Obes Relat Dis. 2012;8(4):371-4. [PubMed: 22480751]

5.

Pournaras DJ, le Roux CW. Obesity, gut hormones, and bariatric surgery. World J Surg. 2009;33(10):1983-8. [PubMed: 19506944]

6.

Carlsson LMS, Sjöholm K, Jacobson P, Andersson-Assarsson JC, Svensson PA, Taube M, et al. Life Expectancy after Bariatric Surgery in the Swedish Obese Subjects Study. N Engl J Med. 2020;383(16):1535-43. [PMC free article: PMC7580786] [PubMed: 33053284]

7.

Mingrone G, Panunzi S, De Gaetano A, Guidone C, Iaconelli A, Capristo E, et al. Metabolic surgery versus conventional medical therapy in patients with type 2 diabetes: 10-year follow-up of an open-label, single-centre, randomised controlled trial. Lancet. 2021;397(10271):293-304. [PubMed: 33485454]

8.

Schauer PR, Bhatt DL, Kirwan JP, Wolski K, Aminian A, Brethauer SA, et al. Bariatric Surgery versus Intensive Medical Therapy for Diabetes - 5-Year Outcomes. N Engl J Med. 2017;376(7):641-51. [PMC free article: PMC5451258] [PubMed: 28199805]

9.

Kashyap SR, Bhatt DL, Wolski K, Watanabe RM, Abdul-Ghani M, Abood B, et al. Metabolic effects of bariatric surgery in patients with moderate obesity and type 2 diabetes: analysis of a randomized control trial comparing surgery with intensive medical treatment. Diabetes Care. 2013;36(8):2175-82. [PMC free article: PMC3714483] [PubMed: 23439632]

10.

Ding SA, Simonson DC, Wewalka M, Halperin F, Foster K, Goebel-Fabbri A, et al. Adjustable Gastric Band Surgery or Medical Management in Patients With Type 2 Diabetes: A Randomized Clinical Trial. J Clin Endocrinol Metab. 2015;100(7):2546-56. [PMC free article: PMC4490302] [PubMed: 25909333]

11.

Halperin F, Ding SA, Simonson DC, Panosian J, Goebel-Fabbri A, Wewalka M, et al. Roux-en-Y gastric bypass surgery or lifestyle with intensive medical management in patients with type 2 diabetes: feasibility and 1-year results of a randomized clinical trial. JAMA Surg. 2014;149(7):716-26. [PMC free article: PMC4274782] [PubMed: 24899464]

12.

Ikramuddin S, Billington CJ, Lee WJ, Bantle JP, Thomas AJ, Connett JE, et al. Roux-en-Y gastric bypass for diabetes (the Diabetes Surgery Study): 2-year outcomes of a 5-year, randomised, controlled trial. The lancet Diabetes & endocrinology. 2015;3(6):413-22. [PMC free article: PMC4477840] [PubMed: 25979364]

13.

Courcoulas AP, Goodpaster BH, Eagleton JK, Belle SH, Kalarchian MA, Lang W, et al. Surgical vs medical treatments for type 2 diabetes mellitus: a randomized clinical trial. JAMA surgery. 2014;149(7):707-15. [PMC free article: PMC4106661] [PubMed: 24899268]

14.

Simonson DC, Halperin F, Foster K, Vernon A, Goldfine AB. Clinical and Patient-Centered Outcomes in Obese Patients With Type 2 Diabetes 3 Years After Randomization to Roux-en-Y Gastric Bypass Surgery Versus Intensive Lifestyle Management: The SLIMM-T2D Study. Diabetes Care. 2018;41(4):670-9. [PMC free article: PMC5860843] [PubMed: 29432125]

15.

Cummings DE, Arterburn DE, Westbrook EO, Kuzma JN, Stewart SD, Chan CP, et al. Gastric bypass surgery vs intensive lifestyle and medical intervention for type 2 diabetes: the CROSSROADS randomised controlled trial. Diabetologia. 2016;59(5):945-53. [PMC free article: PMC4826815] [PubMed: 26983924]

16.

Wentworth JM, Playfair J, Laurie C, Ritchie ME, Brown WA, Burton P, et al. Multidisciplinary diabetes care with and without bariatric surgery in overweight people: a randomised controlled trial. Lancet Diabetes Endocrinol. 2014;2(7):545-52. [PubMed: 24731535]

17.

Dixon JB, O'Brien PE, Playfair J, Chapman L, Schachter LM, Skinner S, et al. Adjustable gastric banding and conventional therapy for type 2 diabetes: a randomized controlled trial. JAMA. 2008;299(3):316-23. [PubMed: 18212316]

18.

Liang Z, Wu Q, Chen B, Yu P, Zhao H, Ouyang X. Effect of laparoscopic Roux-en-Y gastric bypass surgery on type 2 diabetes mellitus with hypertension: a randomized controlled trial. Diabetes Res Clin Pract. 2013;101(1):50-6. [PubMed: 23706413]

19.

Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med. 2008;359(15):1577-89. [PubMed: 18784090]

20.

Kremen A, Linner JH, Nelson CH. An experimental evaluation of the nutritional importance of proximal and distal small intestine. Annals of Surgery. 1954;140:439-44. [PMC free article: PMC1609770] [PubMed: 13198079]

21.

Jorizzo JL, Apisarnthanarax P, Subrt P, Hebert AA, Henry JC, Raimer SS, et al. Bowel-bypass syndrome without bowel bypass. Bowel-associated dermatosis-arthritis syndrome. Archives of Internal Medicine. 1983;143(3):457-61. [PubMed: 6830382]

22.

O'Leary JP. Hepatic complications of jejunoileal bypass. Seminars in Liver Disease. 1983;3(3):203-15. [PubMed: 6353595]

23.

Corrodi P. Jejunoileal bypass: change in the flora of the small intestine and its clinical impact. Reviews of Infectious Diseases. 1984;6 (Suppl 1):S80-4. [PubMed: 6372041]

24.

Parfitt AM, Podenphant J, Villanueva AR, Frame B. Metabolic bone disease with and without osteomalacia after intestinal bypass surgery: a bone histomorphometric study. Bone. 1985;6(4):211-20. [PubMed: 3840379]

25.

DeWind LT, Payne JH. Intestinal bypass surgery for morbid obesity. Long-term results. Journal of the American Medical Association. 1976;236(20):2298-301. [PubMed: 989831]

26.

Mason EE, Ito C. Gastric bypass in obesity. Surgical Clinics of North America. 1967;47(6):1345-51. [PubMed: 6073761]

27.

Printen KJ, Mason EE. Gastric surgery for relief of morbid obesity. Archices of Surgery. 1973;106(4):428-31. [PubMed: 4696714]

28.

Mason EE. Vertical banded gastroplasty for obesity. Archices of Surgery. 1982;117(5):701-6. [PubMed: 7073493]

29.

Hall JC, Watts JM, O'Brien PE, Dunstan RE, Walsh JF, Slavotinek AH, et al. Gastric surgery for morbid obesity. The Adelaide Study. Annals of Surgery. 1990;211(4):419-27. [PMC free article: PMC1358027] [PubMed: 2181950]

30.

Pories WJ, Flickinger EG, Meelheim D, Van Rij AM, Thomas FT. The effectiveness of gastric bypass over gastric partition in morbid obesity: consequence of distal gastric and duodenal exclusion. Annals of Surgery. 1982;196(4):389-99. [PMC free article: PMC1352695] [PubMed: 7125726]

31.

Sugerman HJ, Starkey JV, Birkenhauer R. A randomized prospective trial of gastric bypass versus vertical banded gastroplasty for morbid obesity and their effects on sweets versus non- sweets eaters. Annals of Surgery. 1987;205(6):613-24. [PMC free article: PMC1493086] [PubMed: 3296971]

32.

Sugerman HJ, Londrey GL, Kellum JM, Wolf L, Liszka T, Engle KM, et al. Weight loss with vertical banded gastroplasty and Roux-Y gastric bypass for morbid obesity with selective versus random assignment. American Journal of Surgery. 1989;157(1):93-102. [PubMed: 2910132]

33.

Scopinaro N, Gianetta E, Civalleri D, Bonalumi U, Bachi V. Bilio-pancreatic bypass for obesity: II. Initial experience in man. British Journal of Surgery. 1979;66(9):618-20. [PubMed: 497645]

34.

Scopinaro N, Gianetta E, Adami GF, Friedman D, Traverso E, Marinari GM, et al. Biliopancreatic diversion for obesity at eighteen years. Surgery. 1996;119(3):261-8. [PubMed: 8619180]

35.

Marceau P, Biron S, Bourque RA, Potvin M, Hould FS, Simard S. Biliopancreatic diversion with a new type of gastrectomy. Obesity Surgery. 1993;3(1):29-35. [PubMed: 10757900]

36.

Marceau P, Hould FS, Simard S, Lebel S, Bourque RA, Potvin M, et al. Biliopancreatic diversion with duodenal switch. World Journal of Surgery. 1998;22(9):947-54. [PubMed: 9717420]

37.

Brown WA, Liem R, Al-Sabah S, Anvari M, Boza C, Cohen RV, et al. Metabolic Bariatric Surgery Across the IFSO Chapters: Key Insights on the Baseline Patient Demographics, Procedure Types, and Mortality from the Eighth IFSO Global Registry Report. Obes Surg. 2024;34(5):1764-77. [PMC free article: PMC11031475] [PubMed: 38592648]

38.

Bhandari M, Fobi MAL, Buchwald JN, Group: BMSSBW. Standardization of Bariatric Metabolic Procedures: World Consensus Meeting Statement. Obes Surg. 2019;29(Suppl 4):309-45. [PubMed: 31297742]

39.

Brown WA, Johari Halim Shah Y, Balalis G, Bashir A, Ramos A, Kow L, et al. IFSO Position Statement on the Role of Esophago-Gastro-Duodenal Endoscopy Prior to and after Bariatric and Metabolic Surgery Procedures. Obes Surg. 2020;30(8):3135-53. [PubMed: 32472360]

40.

Zakeri R, Batterham RL. Potential mechanisms underlying the effect of bariatric surgery on eating behaviour. Curr Opin Endocrinol Diabetes Obes. 2018;25(1):3-11. [PubMed: 29120924]

41.

Kalinowski P, Paluszkiewicz R, Wróblewski T, Remiszewski P, Grodzicki M, Bartoszewicz Z, et al. Ghrelin, leptin, and glycemic control after sleeve gastrectomy versus Roux-en-Y gastric bypass-results of a randomized clinical trial. Surg Obes Relat Dis. 2017;13(2):181-8. [PubMed: 27692906]

42.

O'Brien PE, MacDonald L, Anderson M, Brennan L, Brown WA. Long-term outcomes after bariatric surgery: fifteen-year follow-up of adjustable gastric banding and a systematic review of the bariatric surgical literature. Ann Surg. 2013;257(1):87-94. [PubMed: 23235396]

43.

Himpens J, Cadière GB, Bazi M, Vouche M, Cadière B, Dapri G. Long-term outcomes of laparoscopic adjustable gastric banding. Arch Surg. 2011;146(7):802-7. [PubMed: 21422330]

44.

Stefanidis A, Forrest N, Brown WA, Dixon JB, O'Brien PB, Juliane Kampe, et al. An investigation of the neural mechanisms underlying the efficacy of the adjustable gastric band. Surg Obes Relat Dis. 2016;12(4):828-38. [PubMed: 27090808]

45.

Adams TD, Davidson LE, Litwin SE, Kim J, Kolotkin RL, Nanjee MN, et al. Weight and Metabolic Outcomes 12 Years after Gastric Bypass. N Engl J Med. 2017;377(12):1143-55. [PMC free article: PMC5737957] [PubMed: 28930514]

46.

Biter LU, 't Hart JW, Noordman BJ, Smulders JF, Nienhuijs S, Dunkelgrün M, et al. Long-term effect of sleeve gastrectomy vs Roux-en-Y gastric bypass in people living with severe obesity: a phase III multicentre randomised controlled trial (SleeveBypass). Lancet Reg Health Eur. 2024;38:100836. [PMC free article: PMC10835458] [PubMed: 38313139]

47.

Stenberg E, Szabo E, Ågren G, Ottosson J, Marsk R, Lönroth H, et al. Closure of mesenteric defects in laparoscopic gastric bypass: a multicentre, randomised, parallel, open-label trial. Lancet. 2016;387(10026):1397-404. [PubMed: 26895675]

48.

Robert M, Espalieu P, Pelascini E, Caiazzo R, Sterkers A, Khamphommala L, et al. Efficacy and safety of one anastomosis gastric bypass versus Roux-en-Y gastric bypass for obesity (YOMEGA): a multicentre, randomised, open-label, non-inferiority trial. Lancet. 2019;393(10178):1299-309. [PubMed: 30851879]

49.

Mahawar KK, Parmar C, Graham Y. One anastomosis gastric bypass: key technical features, and prevention and management of procedure-specific complications. Minerva Chir. 2019;74(2):126-36. [PubMed: 30019880]

50.

Bolckmans R, Himpens J. Long-term (>10 Yrs) Outcome of the Laparoscopic Biliopancreatic Diversion With Duodenal Switch. Ann Surg. 2016;264(6):1029-37. [PubMed: 26764870]

51.

Sánchez-Pernaute A, Rubio Herrera MA, Pérez-Aguirre E, García Pérez JC, Cabrerizo L, Díez Valladares L, et al. Proximal duodenal-ileal end-to-side bypass with sleeve gastrectomy: proposed technique. Obes Surg. 2007;17(12):1614-8. [PubMed: 18040751]

52.

Torres A, Rubio MA, Ramos-Leví AM, Sánchez-Pernaute A. Cardiovascular Risk Factors After Single Anastomosis Duodeno-Ileal Bypass with Sleeve Gastrectomy (SADI-S): a New Effective Therapeutic Approach? Curr Atheroscler Rep. 2017;19(12):58. [PubMed: 29116413]

53.

Surve A, Cottam D, Medlin W, Richards C, Belnap L, Horsley B, et al. Long-term outcomes of primary single-anastomosis duodeno-ileal bypass with sleeve gastrectomy (SADI-S). Surg Obes Relat Dis. 2020;16(11):1638-46. [PubMed: 32843266]

54.

Sánchez-Pernaute A, Herrera MA, Pérez-Aguirre ME, Talavera P, Cabrerizo L, Matía P, et al. Single anastomosis duodeno-ileal bypass with sleeve gastrectomy (SADI-S). One to three-year follow-up. Obes Surg. 2010;20(12):1720-6. [PubMed: 20798995]

55.

Dijkhorst PJ, Boerboom AB, Janssen IMC, Swank DJ, Wiezer RMJ, Hazebroek EJ, et al. Failed Sleeve Gastrectomy: Single Anastomosis Duodenoileal Bypass or Roux-en-Y Gastric Bypass? A Multicenter Cohort Study. Obes Surg. 2018;28(12):3834-42. [PMC free article: PMC6223754] [PubMed: 30066245]

56.

Ryder REJ, Yadagiri M, Burbridge W, Irwin SP, Gandhi H, Bashir T, et al. Duodenal-jejunal bypass liner for the treatment of type 2 diabetes and obesity: 3-year outcomes in the First National Health Service (NHS) EndoBarrier Service. Diabet Med. 2022;39(7):e14827. [PMC free article: PMC9313821] [PubMed: 35285080]

57.

Pournaras DJ, le Roux CW. Are bile acids the new gut hormones? Lessons from weight loss surgery models. Endocrinology. 2013;154(7):2255-6. [PubMed: 23794408]

58.

Karamanakos SN, Vagenas K, Kalfarentzos F, Alexandrides TK. 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. Ann Surg. 2008;247(3):401-7. [PubMed: 18376181]

59.

Krashes MJ, Koda S, Ye C, Rogan SC, Adams AC, Cusher DS, et al. Rapid, reversible activation of AgRP neurons drives feeding behavior in mice. J Clin Invest. 2011;121(4):1424-8. [PMC free article: PMC3069789] [PubMed: 21364278]

60.

Sohn JW. Network of hypothalamic neurons that control appetite. BMB Rep. 2015;48(4):229-33. [PMC free article: PMC4436859] [PubMed: 25560696]

61.

Farooqi IS, Keogh JM, Yeo GS, Lank EJ, Cheetham T, O'Rahilly S. Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. N Engl J Med. 2003;348(12):1085-95. [PubMed: 12646665]

62.

Sahu A. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Front Neuroendocrinol. 2003;24(4):225-53. [PubMed: 14726256]

63.

Flier JS. Clinical review 94: What's in a name? In search of leptin's physiologic role. J Clin Endocrinol Metab. 1998;83(5):1407-13. [PubMed: 9589630]

64.

Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW, Nyce MR, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292-5. [PubMed: 8532024]

65.

Blüher S, Mantzoros CS. Leptin in humans: lessons from translational research. Am J Clin Nutr. 2009;89(3):991S-7S. [PMC free article: PMC2667664] [PubMed: 19176740]

66.

Nakazato M, Murakami N, Date Y, Kojima M, Matsuo H, Kangawa K, et al. A role for ghrelin in the central regulation of feeding. Nature. 2001;409(6817):194-8. [PubMed: 11196643]

67.

le Roux CW, Neary NM, Halsey TJ, Small CJ, Martinez-Isla AM, Ghatei MA, et al. Ghrelin does not stimulate food intake in patients with surgical procedures involving vagotomy. J Clin Endocrinol Metab. 2005;90(8):4521-4. [PubMed: 15914532]

68.

Tong J, Prigeon RL, Davis HW, Bidlingmaier M, Kahn SE, Cummings DE, et al. Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. Diabetes. 2010;59(9):2145-51. [PMC free article: PMC2927935] [PubMed: 20584998]

69.

Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP, et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002;346(21):1623-30. [PubMed: 12023994]

70.

le Roux CW, Patterson M, Vincent RP, Hunt C, Ghatei MA, Bloom SR. Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects. J Clin Endocrinol Metab. 2005;90(2):1068-71. [PubMed: 15522935]

71.

Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterology. 2007;132(6):2131-57. [PubMed: 17498508]

72.

Deane AM, Nguyen NQ, Stevens JE, Fraser RJ, Holloway RH, Besanko LK, et al. Endogenous glucagon-like peptide-1 slows gastric emptying in healthy subjects, attenuating postprandial glycemia. J Clin Endocrinol Metab. 2010;95(1):215-21. [PubMed: 19892837]

73.

Rocca AS, Brubaker PL. Role of the vagus nerve in mediating proximal nutrient-induced glucagon-like peptide-1 secretion. Endocrinology. 1999;140(4):1687-94. [PubMed: 10098504]

74.

Holz GG, Kühtreiber WM, Habener JF. Pancreatic beta-cells are rendered glucose-competent by the insulinotropic hormone glucagon-like peptide-1(7-37). Nature. 1993;361(6410):362-5. [PMC free article: PMC2916679] [PubMed: 8381211]

75.

Vilsbøll T. The effects of glucagon-like peptide-1 on the beta cell. Diabetes Obes Metab. 2009;11 Suppl 3:11-8. [PubMed: 19878257]

76.

Ørgaard A, Holst JJ. The role of somatostatin in GLP-1-induced inhibition of glucagon secretion in mice. Diabetologia. 2017;60(9):1731-9. [PMC free article: PMC5552842] [PubMed: 28551699]

77.

Tang-Christensen M, Vrang N, Larsen PJ. Glucagon-like peptide containing pathways in the regulation of feeding behaviour. Int J Obes Relat Metab Disord. 2001;25 Suppl 5:S42-7. [PubMed: 11840214]

78.

Batterham RL, Cowley MA, Small CJ, Herzog H, Cohen MA, Dakin CL, et al. Gut hormone PYY(3-36) physiologically inhibits food intake. Nature. 2002;418(6898):650-4. [PubMed: 12167864]

79.

Abbott CR, Monteiro M, Small CJ, Sajedi A, Smith KL, Parkinson JR, et al. The inhibitory effects of peripheral administration of peptide YY(3-36) and glucagon-like peptide-1 on food intake are attenuated by ablation of the vagal-brainstem-hypothalamic pathway. Brain Res. 2005;1044(1):127-31. [PubMed: 15862798]

80.

Sloth B, Holst JJ, Flint A, Gregersen NT, Astrup A. Effects of PYY1-36 and PYY3-36 on appetite, energy intake, energy expenditure, glucose and fat metabolism in obese and lean subjects. Am J Physiol Endocrinol Metab. 2007;292(4):E1062-8. [PubMed: 17148749]

81.

Guo Y, Ma L, Enriori PJ, Koska J, Franks PW, Brookshire T, et al. Physiological evidence for the involvement of peptide YY in the regulation of energy homeostasis in humans. Obesity (Silver Spring). 2006;14(9):1562-70. [PubMed: 17030967]

82.

le Roux CW, Batterham RL, Aylwin SJ, Patterson M, Borg CM, Wynne KJ, et al. Attenuated peptide YY release in obese subjects is associated with reduced satiety. Endocrinology. 2006;147(1):3-8. [PubMed: 16166213]

83.

Batterham RL, Cohen MA, Ellis SM, Le Roux CW, Withers DJ, Frost GS, et al. Inhibition of food intake in obese subjects by peptide YY3-36. N Engl J Med. 2003;349(10):941-8. [PubMed: 12954742]

84.

Claudel T, Staels B, Kuipers F. The Farnesoid X receptor: a molecular link between bile acid and lipid and glucose metabolism. Arterioscler Thromb Vasc Biol. 2005;25(10):2020-30. [PubMed: 16037564]

85.

Ryan KK, Tremaroli V, Clemmensen C, Kovatcheva-Datchary P, Myronovych A, Karns R, et al. FXR is a molecular target for the effects of vertical sleeve gastrectomy. Nature. 2014;509(7499):183-8. [PMC free article: PMC4016120] [PubMed: 24670636]

86.

Bozadjieva N, Heppner KM, Seeley RJ. Targeting FXR and FGF19 to Treat Metabolic Diseases-Lessons Learned From Bariatric Surgery. Diabetes. 2018;67(9):1720-8. [PMC free article: PMC6463577] [PubMed: 30135133]

87.

Alam M, Bhanderi S, Matthews JH, McNulty D, Pagano D, Small P, et al. Mortality related to primary bariatric surgery in England. BJS Open. 2017;1(4):122-7. [PMC free article: PMC5989948] [PubMed: 29951614]

88.

Böckelman C, Hahl T, Victorzon M. Mortality Following Bariatric Surgery Compared to Other Common Operations in Finland During a 5-Year Period (2009-2013). A Nationwide Registry Study. Obes Surg. 2017;27(9):2444-51. [PubMed: 28382506]

89.

Chang SH, Freeman NLB, Lee JA, Stoll CRT, Calhoun AJ, Eagon JC, et al. Early major complications after bariatric surgery in the USA, 2003-2014: a systematic review and meta-analysis. Obes Rev. 2018;19(4):529-37. [PMC free article: PMC5880318] [PubMed: 29266740]

90.

Heneghan HM, Meron-Eldar S, Yenumula P, Rogula T, Brethauer SA, Schauer PR. Incidence and management of bleeding complications after gastric bypass surgery in the morbidly obese. Surg Obes Relat Dis. 2012;8(6):729-35. [PubMed: 21798818]

91.

Gagner M, Kemmeter P. Comparison of laparoscopic sleeve gastrectomy leak rates in five staple-line reinforcement options: a systematic review. Surg Endosc. 2020;34(1):396-407. [PMC free article: PMC6946737] [PubMed: 30993513]

92.

Jacobsen HJ, Nergard BJ, Leifsson BG, Frederiksen SG, Agajahni E, Ekelund M, et al. Management of suspected anastomotic leak after bariatric laparoscopic Roux-en-y gastric bypass. Br J Surg. 2014;101(4):417-23. [PMC free article: PMC4163000] [PubMed: 24536012]

93.

Robertson AGN, Wiggins T, Robertson FP, Huppler L, Doleman B, Harrison EM, et al. Perioperative mortality in bariatric surgery: meta-analysis. Br J Surg. 2021;108(8):892-7. [PubMed: 34297806]

94.

Kermansaravi M, Kassir R, Valizadeh R, Parmar C, Davarpanah Jazi AH, Shahmiri SS, et al. Management of leaks following one-anastomosis gastric bypass: an updated systematic review and meta-analysis of 44 318 patients. Int J Surg. 2023;109(5):1497-508. [PMC free article: PMC10389517] [PubMed: 37026835]

95.

Kim TY, Kim S, Schafer AL, Medical Management of the Postoperative Bariatric Surgery Patient. In Feingold KR, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, et al. Endotext. 2020.

96.

Ekelund M. Systematic review and meta-analysis of internal herniation after gastric bypass surgery (Br J Surg 2015; 102: 451-460). Br J Surg. 2015;102(5):460-1. [PubMed: 25764286]

97.

Farukhi MA, Mattingly MS, Clapp B, Tyroch AH. CT Scan Reliability in Detecting Internal Hernia after Gastric Bypass. JSLS. 2017;21(4). [PMC free article: PMC5740779] [PubMed: 29279662]

98.

Gormsen J, Burcharth J, Gögenur I, Helgstrand F. Prevalence and Risk Factors for Chronic Abdominal Pain After Roux-en-Y Gastric Bypass Surgery: A Cohort Study. Ann Surg. 2021;273(2):306-14. [PubMed: 31058699]

99.

Høgestøl IK, Chahal-Kummen M, Eribe I, Brunborg C, Stubhaug A, Hewitt S, et al. Chronic Abdominal Pain and Symptoms 5 Years After Gastric Bypass for Morbid Obesity. Obes Surg. 2017;27(6):1438-45. [PubMed: 28028658]

100.

DuPree CE, Blair K, Steele SR, Martin MJ. Laparoscopic sleeve gastrectomy in patients with preexisting gastroesophageal reflux disease : a national analysis. JAMA Surg. 2014;149(4):328-34. [PubMed: 24500799]

101.

Peterli R, Wölnerhanssen BK, Peters T, Vetter D, Kröll D, Borbély Y, et al. Effect of Laparoscopic Sleeve Gastrectomy vs Laparoscopic Roux-en-Y Gastric Bypass on Weight Loss in Patients With Morbid Obesity: The SM-BOSS Randomized Clinical Trial. JAMA. 2018;319(3):255-65. [PMC free article: PMC5833546] [PubMed: 29340679]

102.

Parmar CD, Mahawar KK, Boyle M, Schroeder N, Balupuri S, Small PK. Conversion of Sleeve Gastrectomy to Roux-en-Y Gastric Bypass is Effective for Gastro-Oesophageal Reflux Disease but not for Further Weight Loss. Obes Surg. 2017;27(7):1651-8. [PubMed: 28063112]

103.

Robert M, Poghosyan T, Maucort-Boulch D, Filippello A, Caiazzo R, Sterkers A, et al. Efficacy and safety of one anastomosis gastric bypass versus Roux-en-Y gastric bypass at 5 years (YOMEGA): a prospective, open-label, non-inferiority, randomised extension study. Lancet Diabetes Endocrinol. 2024;12(4):267-76. [PubMed: 38452784]

104.

Saarinen T, Pietiläinen KH, Loimaala A, Ihalainen T, Sammalkorpi H, Penttilä A, et al. Bile Reflux is a Common Finding in the Gastric Pouch After One Anastomosis Gastric Bypass. Obes Surg. 2020;30(3):875-81. [PMC free article: PMC7347680] [PubMed: 31853864]

105.

Salminen P, Helmiö M, Ovaska J, Juuti A, Leivonen M, Peromaa-Haavisto P, et al. Effect of Laparoscopic Sleeve Gastrectomy vs Laparoscopic Roux-en-Y Gastric Bypass on Weight Loss at 5 Years Among Patients With Morbid Obesity: The SLEEVEPASS Randomized Clinical Trial. JAMA. 2018;319(3):241-54. [PMC free article: PMC5833550] [PubMed: 29340676]

106.

Wölnerhanssen BK, Peterli R, Hurme S, Bueter M, Helmiö M, Juuti A, et al. Laparoscopic Roux-en-Y gastric bypass versus laparoscopic sleeve gastrectomy: 5-year outcomes of merged data from two randomized clinical trials (SLEEVEPASS and SM-BOSS). Br J Surg. 2021;108(1):49-57. [PubMed: 33640917]

107.

Group B-B-SC. Roux-en-Y gastric bypass, gastric banding, or sleeve gastrectomy for severe obesity: Baseline data from the By-Band-Sleeve randomized controlled trial. Obesity (Silver Spring). 2023;31(5):1290-9. [PubMed: 37140395]

108.

Hedberg S, Olbers T, Peltonen M, Österberg J, Wirén M, Ottosson J, et al. BEST: Bypass equipoise sleeve trial; rationale and design of a randomized, registry-based, multicenter trial comparing Roux-en-Y gastric bypass with sleeve gastrectomy. Contemp Clin Trials. 2019;84:105809. [PubMed: 31279778]

109.

Maciejewski ML, Arterburn DE, Van Scoyoc L, Smith VA, Yancy WS, Weidenbacher HJ, et al. Bariatric Surgery and Long-term Durability of Weight Loss. JAMA Surg. 2016;151(11):1046-55. [PMC free article: PMC5112115] [PubMed: 27579793]

110.

Salminen P, Grönroos S, Helmiö M, Hurme S, Juuti A, Juusela R, et al. Effect of Laparoscopic Sleeve Gastrectomy vs Roux-en-Y Gastric Bypass on Weight Loss, Comorbidities, and Reflux at 10 Years in Adult Patients With Obesity: The SLEEVEPASS Randomized Clinical Trial. JAMA Surg. 2022;157(8):656-66. [PMC free article: PMC9218929] [PubMed: 35731535]

111.

Carandina S, Soprani A, Zulian V, Cady J. Long-Term Results of One Anastomosis Gastric Bypass: a Single Center Experience with a Minimum Follow-Up of 10 Years. Obes Surg. 2021;31(8):3468-75. [PubMed: 34097238]

112.

Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222(3):339-50; discussion 50-2. [PMC free article: PMC1234815] [PubMed: 7677463]

113.

Rubino F, Nathan DM, Eckel RH, Schauer PR, Alberti KG, Zimmet PZ, et al. Metabolic Surgery in the Treatment Algorithm for Type 2 Diabetes: A Joint Statement by International Diabetes Organizations. Diabetes Care. 2016;39(6):861-77. [PubMed: 27222544]

114.

Courcoulas AP, Patti ME, Hu B, Arterburn DE, Simonson DC, Gourash WF, et al. Long-Term Outcomes of Medical Management vs Bariatric Surgery in Type 2 Diabetes. JAMA. 2024;331(8):654-64. [PMC free article: PMC10900968] [PubMed: 38411644]

115.

Dixon JB, O'Brien PE, Playfair J, Chapman L, Schachter LM, Skinner S, et al. Adjustable gastric banding and conventional therapy for Type 2 Diabetes: A randomized controlled trial. Journal of the American Medical Association. 2008;299(3):316-23. [PubMed: 18212316]

116.

Mingrone G, Panunzi S, De Gaetano A, Guidone C, Iaconelli A, Nanni G, 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 controlled trial. Lancet. 2015;386(9997):964-73. [PubMed: 26369473]

117.

Kirwan JP, Courcoulas AP, Cummings DE, Goldfine AB, Kashyap SR, Simonson DC, et al. Diabetes Remission in the Alliance of Randomized Trials of Medicine Versus Metabolic Surgery in Type 2 Diabetes (ARMMS-T2D). Diabetes Care. 2022;45(7):1574-83. [PMC free article: PMC9490448] [PubMed: 35320365]

118.

Ikramuddin S, Korner J, Lee WJ, Connett JE, Inabnet WB, Billington CJ, 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. [PMC free article: PMC3954742] [PubMed: 23736733]

119.

Schauer PR, Bhatt DL, Kirwan JP, Wolski K, Brethauer SA, Navaneethan SD, et al. Bariatric surgery versus intensive medical therapy for diabetes--3-year outcomes. N Engl J Med. 2014;370(21):2002-13. [PMC free article: PMC5451259] [PubMed: 24679060]

120.

Sjostrom L, Peltonen M, Jacobson P, Ahlin S, Andersson-Assarsson J, Anveden A, et al. Association of Bariatric Surgery With Long-term Remission of Type 2 Diabetes and With Microvascular and Macrovascular Complications. JAMA. 2014;311(22):2297-304. [PubMed: 24915261]

121.

Sjöström L, Gummesson A, Sjöström CD, Narbro K, Peltonen M, Wedel H, et al. Effects of bariatric surgery on cancer incidence in obese patients in Sweden (Swedish Obese Subjects Study): a prospective, controlled intervention trial. Lancet Oncol. 2009;10(7):653-62. [PubMed: 19556163]

122.

Aminian A, Wilson R, Al-Kurd A, Tu C, Milinovich A, Kroh M, et al. Association of Bariatric Surgery With Cancer Risk and Mortality in Adults With Obesity. JAMA. 2022;327(24):2423-33. [PMC free article: PMC9166218] [PubMed: 35657620]

123.

Clapp B, Portela R, Sharma I, Nakanishi H, Marrero K, Schauer P, et al. Risk of non-hormonal cancer after bariatric surgery: meta-analysis of retrospective observational studies. Br J Surg. 2022;110(1):24-33. [PubMed: 36259310]

124.

Aminian A, Zajichek A, Arterburn DE, Wolski KE, Brethauer SA, Schauer PR, et al. Association of Metabolic Surgery With Major Adverse Cardiovascular Outcomes in Patients With Type 2 Diabetes and Obesity. JAMA. 2019. [PMC free article: PMC6724187] [PubMed: 31475297]

125.

Lazo M, Clark JM. The epidemiology of nonalcoholic fatty liver disease: a global perspective. Semin Liver Dis. 2008;28(4):339-50. [PubMed: 18956290]

126.

Caldwell S, Argo C. The natural history of non-alcoholic fatty liver disease. Dig Dis. 2010;28(1):162-8. [PubMed: 20460906]

127.

Bzowej NH. Nonalcoholic steatohepatitis: the new frontier for liver transplantation. Curr Opin Organ Transplant. 2018;23(2):169-74. [PubMed: 29356708]

128.

Fakhry TK, Mhaskar R, Schwitalla T, Muradova E, Gonzalvo JP, Murr MM. Bariatric surgery improves nonalcoholic fatty liver disease: a contemporary systematic review and meta-analysis. Surg Obes Relat Dis. 2019;15(3):502-11. [PubMed: 30683512]

129.

Despres J. The insulin resistance-dyslipidemia syndrome: The most prevalent cause of coronary artery disease. Canadian Medical Association Journal. 1993;148(8):1339-40. [PMC free article: PMC1491750] [PubMed: 8462056]

130.

Koba S, Hirano T, Sakaue T, Sakai K, Kondo T, Yorozuya M, et al. Role of small dense low-density lipoprotein in coronary artery disease patients with normal plasma cholesterol levels. Journal of Cardiology. 2000;36(6):371-8. [PubMed: 11190580]

131.

Busetto L, Pisent C, Rinaldi D, Longhin PL, Segato G, De Marchi F, et al. Variation in lipid levels in morbidly obese patients operated with the LAP-BAND adjustable gastric banding system: effects of different levels of weight loss. Obesity Surgery. 2000;10(6):569-77. [PubMed: 11175968]

132.

Bacci V, Basso MS, Greco F, Lamberti R, Elmore U, Restuccia A, et al. Modifications of metabolic and cardiovascular risk factors after weight loss induced by laparoscopic gastric banding. Obesity Surgery. 2002;12(1):77-82. [PubMed: 11868304]

133.

Dixon J, O'Brien P. Ovarian dysfunction, androgen excess and neck circumference in obese women: Changes with weight loss (abstract). Obesity Surgery. 2002;12(2):193. [PubMed: 17476870]

134.

Brolin RE, Bradley LJ, Wilson AC, Cody RP. Lipid risk profile and weight stability after gastric restrictive operations for morbid obesity. Journal of Gastrointestinal Surgery. 2000;4(5):464-9. [PubMed: 11077320]

135.

Carbajo MA, Fong-Hirales A, Luque-de-León E, Molina-Lopez JF, Ortiz-de-Solórzano J. Weight loss and improvement of lipid profiles in morbidly obese patients after laparoscopic one-anastomosis gastric bypass: 2-year follow-up. Surg Endosc. 2017;31(1):416-21. [PubMed: 27317038]

136.

Sjostrom CD, Lissner L, Wedel H, Sjostrom L. Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study. Obesity Research. 1999;7(5):477-84. [PubMed: 10509605]

137.

Schiavon CA, Cavalcanti AB, Oliveira JD, Machado RHV, Santucci EV, Santos RN, et al. Randomized Trial of Effect of Bariatric Surgery on Blood Pressure After 5 Years. J Am Coll Cardiol. 2024;83(6):637-48. [PubMed: 38325988]

138.

Beuther DA, Sutherland ER. Overweight, obesity, and incident asthma: a meta-analysis of prospective epidemiologic studies. American Journal of Respiratory and Critical Care Medicine. 2007;175(7):661-6. [PMC free article: PMC1899288] [PubMed: 17234901]

139.

Young SY, Gunzenhauser JD, Malone KE, McTiernan A. Body mass index and asthma in the military population of the northwestern United States. Archives of Internal Medicine. 2001;161(13):1605-11. [PubMed: 11434792]

140.

Camargo C, Weiss S, Zhang S, Willett W, Speizer F. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med. 1999;159(Nov):2582-88. [PubMed: 10573048]

141.

Diaz J, Farzan S. Clinical implications of the obese-asthma phenotypes. Immunol Allergy Clin North Am. 2014;34(4):739-51. [PubMed: 25282287]

142.

Khalooeifard R, Adebayo R, Rahmani J, Clark C, Shadnoush M, Mohammadi Farsani G. Health Effect of Bariatric Surgery on Patients with Asthma: A Systematic Review and Meta-Analysis. Bariatric Surgical Practice and Patient Care. 2021;16(1):2-9.

143.

Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284(23):3015-21. [PubMed: 11122588]

144.

Camargo CA, Weiss ST, Zhang S, Willett WC, Speizer FE. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med. 1999;159(21):2582-8. [PubMed: 10573048]

145.

Dixon JB. Elevated homocysteine with weight loss. Obesity Surgery. 2001;11(5):537-8. [PubMed: 11594089]

146.

Weiner R, Datz M, Wagner D, Bockhorn H. Quality-of-life outcome after laparoscopic adjustable gastric banding for morbid obesity. Obesity Surgery. 1999;9(6):539-45. [PubMed: 10638479]

147.

Schok M, Geenen R, van Antwerpen T, de Wit P, Brand N, van Ramshorst B. Quality of life after laparoscopic adjustable gastric banding for severe obesity: postoperative and retrospective preoperative evaluations. Obesity Surgery. 2000;10(6):502-8. [PubMed: 11175956]

148.

Balsiger BM, Kennedy FP, Abu-Lebdeh HS, Collazo-Clavell M, Jensen MD, O'Brien T, et al. Prospective evaluation of Roux-en-Y gastric bypass as primary operation for medically complicated obesity [see comments]. Mayo Clinic Proceedings. 2000;75(7):673-80. [PubMed: 10907381]

149.

Horchner R, Tuinebreijer MW, Kelder PH. Quality-of-life assessment of morbidly obese patients who have undergone a Lap-Band operation: 2-year follow-up study. Is the MOS SF- 36 a useful instrument to measure quality of life in morbidly obese patients? Obesity Surgery. 2001;11(2):212-8; discussion 9. [PubMed: 11355029]

150.

O'Brien P, Brown W, Dixon J. Revisional Surgery for Morbid Obesity- Conversion to the Lap-Band System. Obesity Surgery. 2000;10(6):557-63. [PubMed: 11175966]

151.

Syn NL, Cummings DE, Wang LZ, Lin DJ, Zhao JJ, Loh M, et al. Association of metabolic-bariatric surgery with long-term survival in adults with and without diabetes: a one-stage meta-analysis of matched cohort and prospective controlled studies with 174 772 participants. Lancet. 2021;397(10287):1830-41. [PubMed: 33965067]

152.

Pournaras DJ, Hardwick RH, le Roux CW. Gastrointestinal surgery for obesity and cancer: 2 sides of the same coin. Surg Obes Relat Dis. 2017;13(4):720-1. [PubMed: 28161354]

153.

Sudlow A, le Roux CW, Pournaras DJ. Review of multimodal treatment for type 2 diabetes: combining metabolic surgery and pharmacotherapy. Ther Adv Endocrinol Metab. 2019;10:2042018819875407. [PMC free article: PMC6759694] [PubMed: 31579501]

154.

NIH conference. Gastrointestinal surgery for severe obesity. Consensus Development Conference Panel. Ann Intern Med. 1991;115(12):956-61. [PubMed: 1952493]