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Curr Diab Rep. Author manuscript; available in PMC 2020 September 29.
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Published in final edited form as:

Curr Diab Rep. ; 19(12): 156. doi:10.1007/s11892-019-1269-4.

Bariatric Surgery in the Treatment of Type 2 Diabetes

Alison H. Affinati1, Nazanene H. Esfandiari1, Elif A. Oral1, Andrew T. Kraftson1
1Divisionof Metabolism, Endocrinology and Diabetes (MEND), Department of Internal Medicine,
Michigan Medicine, University of Michigan, 24 Frank Lloyd Wright Drive, Lobby G, Suite 1500,
Ann Arbor, MI 48106-0482, USA

Abstract
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Purpose of Review—We seek to characterize the impact of bariatric surgery on diabetes

mellitus by recalling its history, examining the clinical data, exploring the putative mechanisms of
action, and anticipating its future.

Recent Findings—Results of clinical trials reveal that bariatric surgery induces remission of
diabetes in 33–90% of individuals at 1-year post-treatment versus 0–39% of medically managed.
Remission rates decrease over time but remain higher in surgically treated individuals.
Investigations have revealed numerous actions of surgery including effects on intestinal
physiology, neuronal signaling, incretin hormone secretion, bile acid metabolism, and microbiome
changes.

Summary—Bariatric surgery improves control of diabetes through both weight-dependent and

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weight-independent actions. These various mechanisms help explain the difference between
individuals treated surgically vs. medically. They also explain differing effects of various bariatric
surgery procedure types. Understanding how surgery affects diabetes will help optimize utilization
of the therapy for both disease prevention and treatment.

Keywords
Bariatric surgery; Metabolic surgery; Diabetes mellitus; Diabetes remission; Obesity

Introduction
“Diabesity” was coined in 1973 to emphasize the pathophysiologic interconnection between
the diseases of type 2 diabetes and obesity [1, 2]. Since that time, the acceleration of
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diabesity’s impact on health and economics has led Dr. Paul Zimmet to state that it “is likely
to be the biggest epidemic in human history” [3]. Worldwide, 650 million individuals have
the disease of obesity and over 400 million individuals have diabetes [4, 5]. The impact of
these diseases on morbidity, mortality, quality of life, and healthcare costs have been well-

Andrew T. Kraftson, andrewkr@med.umich.edu.

This article is part of the Topical Collection on Therapies and New Technologies in the Treatment of Diabetes
Conflict of Interest Alison H. Affinati, Nazanene H. Esfandiari, and Andrew T. Kraftson declare that they have no conflict of interest.
Human and Animal Rights and Informed Consent All procedures performed in studies involving human participants were in
accordance with the ethical standards of the institutional and/or national research committee (include name of committee + reference
number) and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
 Affinati et al. Page 2

described [6]. Treating individuals with diabetes and obesity results in health improvements
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and long-term reductions in healthcare costs [7–9]. Unfortunately, significant health

improvements can be difficult to attain and/or maintain even with the best available dietary,
behavioral, and medication therapies available [2]. As an illustration of this point, the results
of a study examining the 2012 claims data from the 50 largest metropolitan areas in the USA
revealed that 44% of insured patients diagnosed with diabetes and receiving medication
therapy were classified as having “uncontrolled” diabetes [10]. Similarly, conventional,
lifestyle-focused weight management strategies face challenges in terms of degree of weight
loss, weight maintenance, and attrition [11, 12]. Furthermore, individuals with both obesity
and diabetes tend to lose less weight and have more difficulty maintaining a reduced-weight
state when compared to individuals without diabetes [13, 14]. As such, there has been a
pressing need for therapeutic options beyond the traditional medical tools. Bariatric surgery
has emerged as the most effective treatment for weight loss and maintenance.
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Unsurprisingly, it is also being recognized as a highly effective treatment for type 2 diabetes
[15]. Interestingly, the mechanisms by which surgery impacts glucose homeostasis are much
more extensive than originally expected and continue to be elucidated. In this review, we
will describe the clinical problem, the impact of bariatric surgery on diabetes, the
physiologic mechanisms for the glycemic effects of surgery, and emerging policy
discussions.

Obesity and Diabetes

The connection between obesity and type 2 diabetes has long been recognized [1].
Observationally, the rise in incidence and prevalence of diabetes has mirrored the rise in
obesity prevalence rates [16, 17]. However, even though 90% of individuals with type 2
diabetes are obese, a substantially smaller fraction of individuals with obesity develop
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diabetes [4]. Yet, obesity is thought to be the strongest risk factor for development of type 2
diabetes [18]. This observation can be explained through an understanding of the biology of
these diseases. Obesity is associated with various pathophysiologic changes that increase
insulin resistance [19]. Despite the increase in insulin demand and decrease in insulin
sensitivity, the pancreas can normally compensate by increasing insulin production to
maintain glucose homeostasis. In contrast, when an individual with the genetic
predisposition for type 2 diabetes is exposed to obesogenic environmental factors (increased
fat/carbohydrate/caloric intake; decreased physical activity), pancreatic beta-cell
dysfunction, altered adipose tissue function, and weight gain can occur [20]. The
combination of progressively declining insulin production capacity and rising insulin
resistance results in the inability of the body to maintain euglycemia. Eventually, this can be
detected as impaired glucose tolerance and, later, clinical type 2 diabetes [19, 21]. Given the
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intersection between these processes, weight reduction has been the foundational treatment
recommendation for individuals diagnosed with both obesity and diabetes [22].
Unfortunately, conventional methods to facilitate weight loss are unsuccessful for the
majority of individuals [2]. Furthermore, many anti-diabetes medications such as insulin,
sulfonylureas, meglitinides, and thiazolidinediones are associated with weight gain [23, 24].
Consequently, many individuals with diabetes remain in a vicious cycle where treatments for
hyperglycemia can complicate long-term care by exacerbating obesity. Fortunately, weight-

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negative anti-diabetes treatment options such as glucagon-like peptide-1 receptor agonists

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(GLP-1 RA) and sodium glucose transporter-2 inhibitors have become available [25]. Yet,
the magnitude of the weight loss seen with use of these medications is often insufficient to
address severe obesity [26, 27].

After years of observing that shortened guts were associated with weight loss, surgeons in
the 1950s started to develop surgical procedures to treat obesity [15]. Over the ensuing
decades, surgical options have evolved in pursuit of the goal of optimizing both safety and
efficacy. The types of bariatric surgery are reviewed in Table 1 [28–30].

As of 2019, the most commonly performed surgeries are sleeve gastrectomy (SG), Roux-en-
Y gastric bypass (RYGB), laparoscopic adjustable gastric band (LAGB), and biliopancreatic
diversion with duodenal switch (BPD/DS) [28]. As the techniques have changed and
matured, the understanding of the mechanisms by which surgery facilitates weight loss and
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maintenance of a reduced-weight state has also evolved. At first, weight loss was thought to
occur primarily through caloric restriction and/or malabsorption and surgical procedures
were categorized based on these presumed mechanisms of action. It is now recognized that
most of the current, commonly performed surgeries improve both obesity and its
comorbidities (including type 2 diabetes) through pleiotropic effects on intestinal
physiology, transcriptional programs in intestinal differentiation programs, neuronal
signaling, incretin hormone secretion, bile acid metabolism, lipid regulation, microbiome
changes, and glucose homeostasis. For this reason, many prefer to describe these procedures
as types of “metabolic surgery” [31, 32]. These observations have led to intensified efforts to
assess the impact of surgery on type 2 diabetes and better understand the mechanisms behind
its effects.
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Impact of Surgery on Type 2 Diabetes

Given the long-recognized association of type 2 diabetes and obesity, it was expected that
glycemic control would improve as a result of surgically facilitated weight loss. However,
the surprising observation of immediate, post-surgical glycemic improvement suggested
short-term mechanisms of action that were distinct from (but complementary to) long-term
mechanisms. These provocative anecdotal accounts and ensuing case reports paved the way
for several cohort studies published in the 1980s that helped explore the impact of bariatric
surgery on type 2 diabetes in both the short and long term. For example, one study of
insulin-treated patients with type 2 diabetes recorded an improvement in glycated
hemoglobin (HbA1c) from 11.8 to 7.9% following gastric bypass surgery and another study
noted 139 of 141 patients were able to discontinue anti-diabetes medications by 4-month
post-surgery [33, 34].
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These early studies stimulated efforts to quantify the impact of bariatric surgery on type 2
diabetes. Consequently, metrics were needed as part of the assessment process. The chief
metric that has emerged is the rate of inducing “diabetes remission.” Unfortunately, there
has not been consensus on the definition of the term and the ensuing variations complicate
review of the data. For example, some early cohort studies defined remission as medication-
free euglycemia (i.e., normal range fasting blood sugar and/or HbA1c) while others allowed
for continued monotherapy with metformin [35–37]. In 2009, the American Diabetes

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Association (ADA) published a consensus statement defining complete diabetes remission

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as demonstrating normal fasting blood glucose levels and/or HbA1c without the use of anti-
diabetes medications for at least 1 year. Partial remission was defined as HbA1c < 6.5% and
fasting blood glucose less than 126 mg/dL without medications for 1 year [38]. Since then,
many of recent studies have used similar definitions [39–42•]. Of note, at the time of
manuscript submission, the upcoming revised ADA consensus statement on diabetes
remission was still under development.

Regardless of the definitions used, clinical studies have repeatedly demonstrated the
significant ability of surgery to improve glucose homeostasis and induce remission. Several
large cohort studies comparing bariatric surgery to conventional obesity management have
confirmed that bariatric surgery patients are able to achieve diabetes remission more
frequently than those who use conventional obesity therapy alone [35–37, 43•, 44•]. For
example, in the Swedish Obesity Study (SOS), of 343 patients that underwent bariatric
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surgery (VBG, LAGB, and RYGB), 72.4% achieved diabetes remission at 2 years, compared
to only 16.4% of control patients [35]. Similarly, in a 2019 study that included 1111 patients
with diabetes who underwent RYGB, 74% of patients had diabetes remission at 1 year [44•].

While cohort studies provide evidence that bariatric surgery can induce diabetes remission,
they may be confounded by factors inherent to the patients that choose bariatric surgery over
medical therapy. Additionally, some cohort studies use conventional obesity therapy, which
may not include a rigorous, validated weight loss program as the control group [35, 44•],
leading to under-estimation of the effectiveness of medical therapy and inflation of the
efficacy of bariatric surgery. To address these concerns and improve scientific understanding,
randomized controlled trials (RCTs) were conducted. These have been designed to compare
the effectiveness of bariatric surgery and lifestyle/medical management to induce diabetes
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remission. The results of significant trials (cohort and RCT) are summarized in Table 2.

As seen by the studies summarized, there is a wide range of remission rates reported after
surgical therapy. The heterogeneity is likely due to the diversity of surgical procedures
included, the varied populations studied, and the different definitions of diabetes remission
used. Additionally, studies can vary with respect to reporting cumulative remission (counted
as any individual who ever achieved remission) and/or prevalent remission (counted as only
individuals who were in remission at the time of measurement). Furthermore, some studies
correct for attrition while others do not [54]. Despite this variability, the RCTs consistently
demonstrate that bariatric surgery has a superior diabetes remission rate when compared to
medical therapy. For example, after 1 year of treatment, diabetes remits in a substantial
proportion (33–90%) of surgically managed individuals but only in a small minority (0–
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39%) of medically managed individuals (Table 2). As further evidence of this, a meta-
analysis of clinical trials available through 2013 (with follow-up ranging from 40 weeks to 2
years) concluded that the relative risk of attaining diabetes remission was at least 5 times
higher in surgically treated individuals versus non-surgical groups and possibly as much as
22 times higher [55].

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Diabetes and Bariatric Surgery: Mechanisms

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As the results of the numerous clinical studies have accumulated, many clinical and
scientific questions have arisen. The most fundamental of these is: why does diabetes
improve after surgery? In keeping with expectations, some degree of glycemic improvement
after bariatric surgery is associated with weight loss. Indeed, 75% of patients who did not
achieve diabetes remission had weight regain [47]. Insulin sensitivity, a crucial component
of diabetes pathogenesis, improves in patients following bariatric surgery to a similar degree
as in patients who have lost an equivalent amount of weight using caloric restriction [57, 59,
61]. The weight-dependence of improved insulin sensitivity is further supported in studies
comparing SG and RYGB, which have differing effects on gut physiology. In patients that
achieved 20% weight loss, both SG patients and RYGB patients achieved similar
improvements in insulin sensitivity [62].
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Somewhat less expected has been the discovery that the microbiome may contribute to
improvement in glucose homeostasis following bariatric surgery. While it is unclear if
changes in the gut microbiome cause metabolic improvement, or occur because of metabolic
improvement, the gut microbiome is markedly altered following bariatric surgery with
increased microbiome diversity within 3 months [63–66] in both RYGB and VBG. In
rodents, fecal transplant from either mice or humans that have undergone RYGB into germ-
free rats fed a high-fat diet results in weight loss and improvement in glycemic parameters,
suggesting that, regardless of what causes the microbiome to change, the post-RYGB
microbiome improves glycemic control [67, 68].

A striking feature of bariatric surgery is the rapid improvement in glycemic control that
precedes weight loss. In some of the earliest case reports, authors remarked that some
patients were insulin-free at the time of discharge despite having pre-surgical insulin
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requirements of hundreds of units [34]. What are the mechanisms that drive these rapid,
weight-independent improvements in glucose homeostasis? The answer to this question is
rather complex but starts with alterations in gut hormones which are worth reviewing here.

Glucagon-like peptide 1 (GLP-1) is a gut hormone secreted from intestinal neuroendocrine

L cells which induces the “incretin effect” of increasing insulin secretion and glucose
clearance in response to oral glucose. Following bariatric surgery, post-prandial GLP-1
levels are increased, leading to improved beta-cell glucose sensitivity and lower post-
prandial blood glucose [69–72]. In mice lacking the GLP-1 receptor (GLP-1R KO mice),
continued improvements in glucose homeostasis following SG and RYGB are observed [73–
75], as occurs in patients treated with a GLP-1 receptor antagonist following bariatric
surgery [76].
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Other gut hormones that may contribute to improved glucose homeostasis include PYY and
oxyntomodulin, both of which are increased following bariatric surgery. Indeed, a recent
clinical trial of subcutaneous GLP-1, PYY, and oxyntomodulin combination therapy for 4
weeks demonstrated improved post-prandial glycemic control similar to that of RYGB
patients [77].

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As practice patterns evolved and as SG has superseded RYGB as the most commonly
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performed bariatric surgery [28], most recent studies have focused on comparisons between
these two procedures. Based on these studies, it appears that patients who undergo “more”
rearrangement of their GI tract have a small, but reproducible, improvement in long-term
glycemic control compared to patients undergoing less drastic procedures. This is
demonstrated by a recent meta-analysis that reviewed 16 RCTs comparing glycemic
outcomes in patients who underwent SG versus RYGB and found that patients who
underwent RYGB had lower fasting blood sugar and lower A1c at 3 years following surgery
[78•]. In further support of this hypothesis, the lowest remission rate is reported for LAGB,
which does not alter the gut anatomy, with a 1-year diabetes remission rate of 33% [79].

Why do some procedure types affect glycemic control more than others? Historically, two
competing (but not mutually exclusive) hypotheses have emerged to explain how gut
rearrangement leads to improvements in glycemic control: the hindgut hypothesis and the
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foregut-exclusion hypothesis.

The hindgut hypothesis states that bypassing the proximal small bowel causes rapid transit
of nutrients into the distal bowel, increasing secretion of gut hormones such as GLP-1 and
PYY. This is supported by rodent studies in which anastomosing the ileum to the proximal
bowel increases gut transit time [80], while post-surgical GLP-1 levels are higher in rats that
underwent RYGB than in those that underwent SG [81].

The foregut-exclusion hypothesis posits that exclusion of nutrients from the duodenum and
proximal jejunum decreases secretion of an as-yet unidentified signal that increases insulin
resistance. This hypothesis has been tested in rodent studies as well. Rats received either
duodenojejunal bypass, which completely excludes nutrients from the duodenum and
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proximal jejunum, or gastrojejunostomy, in which nutrients are able to rapidly reach the
distal jejunum, but still have access to the duodenum. Rats that underwent duodenal-jejunal
bypass had a significant improvement in their glucose tolerance, while the
gastrojejunostomy rats did not, leading to the proposal of “anti-incretin” factors secreted
from the duodenum [82]. Based on these findings, less invasive metabolic surgeries are now
under investigation that simply ablates the duodenal mucosa, known as duodenal mucosal
resurfacing [83].

Another metabolic pathway that is altered following rearrangement of the gut is bile acid
signaling. Serum bile acid concentrations and composition change following RYGB and SG,
but not following LAGB. Bile acids act as hormones that bind to the hormone receptor FXR
and lead to improvements in glucose tolerance [84–89]. In rodent studies, improvements in
glucose tolerance following VSG are reduced in mice lacking FXR or its binding partner
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TGR5 [88, 89]. However, pharmacologic studies in rodents have also shown that both
inhibition and activation of FXR result in improved metabolic phenotypes accompanied by
weight loss, thus the specific effect of activating FXR-signaling is unclear.

Failure to Achieve Diabetes Remission and Relapse of Diabetes

While bariatric surgery clearly demonstrates a high ability to induce remission of type 2
diabetes, the clinical trial data also reveal that remission is not attained in all individuals.

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Understanding the factors that predict glycemic response to surgery is critical in determining
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which patients are most likely to achieve diabetes remission. Several studies have addressed
this question and the factors that are most associated with diabetes remission include shorter
duration of diabetes prior to surgery (< 4 years), higher C-peptide, younger age, and use of
only oral agents or diet to control diabetes [90–93]. While these collective data demonstrate
the short-term efficacy of bariatric surgery, the durability of diabetes remission remains a
pressing clinical question. Even though the majority of individuals will have long-term
improvements in diabetes metrics (i.e., HbA1c < 7%, reduction in anti-diabetes medications,
and reduction in complication rates), sustained remission is experienced by only a minority.
Studies evaluating long-term outcomes have demonstrated an almost 50% relapse rate for
patients who achieve diabetes remission [39, 44•, 47, 48, 50]. For example, 15-year follow-
up data from the SOS revealed that rates of diabetes remission (defined as blood glucose
levels under 110 mg/dL without anti-diabetes medication use) drop from 72.4% at 2 years
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post-surgery to 38.1% at 10 years and further to 30.4% at 15 years [60]. This is replicated in
RCTs, as well. In a 2015 study conducted by Mingrone and colleagues in which individuals
were randomized to medical therapy (n = 20), RYGB (n = 20), or BPD (n = 20), ADA
partial remission was achieved at 2 years in 0, 75%, and 95% of individuals in these
respective groups. By 5 years, the rates were 0, 37%, and 63% [47]. The factors that predict
remission also contribute to achieving sustained remission. Predictors of relapse include
insulin use and a longer duration of diabetes prior to surgery, with an HR of 1.13 for every
additional prior year of having a diabetes diagnosis [39].

Impact of Bariatric Surgeryon Diabetes-Related Complications and

Prevention
While diabetes remission rates are an important metric for assessing bariatric surgery’s
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impact on type 2 diabetes, health benefits are not exclusively conferred to individuals
attaining remission. Multiple cohort studies and RCTs demonstrate that patients who
undergo bariatric surgery experience a significant reduction in the use of both oral anti-
diabetic medications and insulin. In one study, there was an 87% reduction in oral
medication use and a 79% reduction in patients who continue to require insulin [36, 41, 47,
49•]. Our own data from a real world setting suggest 68.7% vs 56.0% reduction in diabetes
medication usage after GB versus SG [52•]. Moreover, the years spent in good control are
known to have a legacy effect for the subsequent decade in terms of fewer diabetes
complications. Therefore, it is not surprising that bariatric surgery is also associated with a
decreased incidence rate of both diabetes-related microvascular and macrovascular
complications and decreased mortality. In the 15-year follow-up of the SOS, microvascular
complications were 20.6 per 1000 person-years in the surgical patients as compared to 41.8
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per 1000 person-years in controls (HR of 0.44 for the surgical patients). Additionally,
macrovascular complications were also lower in the surgical group (31.7 per 1000 person-
years) as compared to the control group (44.2 per 1000 person-years) with an HR of 0.68 for
surgical patients. Perhaps most importantly, this study and several others have also shown
decreased long-term mortality in surgical patients [60, 94, 95].

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Studies have also examined the effect of bariatric surgery on prevention of diabetes
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development. In the SOS trial, bariatric surgery reduced the risk of developing diabetes by
96% at 2 years post-intervention and 78% at 15 years [60, 96]. Given the data on
complications and prevention, bariatric surgery is being recognized as a valuable tool for
disease and complication prevention, not just treatment [97].

Bariatric Surgery: Diabetes Treatment Guidelines

Globally, consideration for bariatric surgery generally occurs for individuals that meet the
1991 National Institutes of Health (NIH) criteria [98]. Qualifying individuals must have a
body mass index (BMI) ≥ 40 kg/m2 or BMI ≥ 35 with a serious weight-related comorbid
health condition (such as diabetes). Yet, studies such as the STAMPEDE trial have included
participants with lower BMIs than the NIH criteria and provided evidence of benefit for
these patients [49•].
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Based on the growing body of evidence and the expanded understanding of the mechanisms
of actions of metabolic surgeries, there has been a growing movement to expand the
eligibility criteria for surgery. In 2016, the 2nd Diabetes Surgery Summit (DSS-II) was
convened which led to a consensus statement for the use of surgery as a primary treatment
method for type 2 diabetes. A joint statement of the partner societies (including the ADA,
the International Diabetes Federation, Diabetes UK, the Chinese Diabetes Society, and
Diabetes India) was released and called for bariatric surgery to be “considered in patients
with class I obesity (BMI 30.0–34.9) and inadequately controlled hyperglycemia despite
optimal medical treatment by either oral or injectable medications (including insulin)” [99].
This statement falls short of acknowledging the racial and ethnic differences of adiposity and
the resulting metabolic complications across populations of the world. It will be interesting
to see if the improved understanding of these differences will lead to recommendations for
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surgical interventions at lower adiposity ranges in populations where metabolic

consequences of increased adiposity are noted at much lower BMI levels.

Conclusion
Diabetes and obesity pose individual and global health challenges to a scale that is
unprecedented. While many conventional medical therapeutic options are available, they are
not universally effective due to myriad physiological, behavioral, and financial barriers.
Bariatric surgery has emerged as the single most effective treatment option for type 2
diabetes and obesity. It must be acknowledged that surgery does not address the fundamental
problem of overabundance of energy availability. Yet, though not a panacea for the
environmental challenges, or a cure for these diseases, surgery significantly decreases their
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burden through weight-dependent and weight-independent mechanisms. Furthermore,

elucidating these mechanisms improves the understanding of the diseases, themselves.
Consequently, bariatric surgery serves as both an illuminating scientific model and an
effective treatment tool to address the diabesity crisis.

Funding Information
Alison H. Affinati reports a grant from NIDDK (F32 DK122660).

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Elif A. Oral reports grants from Gi Dynamics; grants, personal fees, and non-financial support from Aegerion
Pharmaceuticals; grants and personal fees from Akcea Therapeutics; grants from Ionis Pharmaceuticals; grants and
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personal fees from Regeneron Pharmaceuticals; and grants from Gemphire Therapeutics. In addition, Dr. Oral has a
patent issue on an Intragastric device.

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Table 1

Types of bariatric surgery procedures

Surgery type Description Time introduced Estimated % of total

bariatric cases
Affinati et al.

performed from 2011 to

2017
Jejunoileal bypass (JIB) Bypass of most of the intestines with gastric preservation 1950s 0 (no longer performed)
Roux-en-Y gastric bypass (RYGB) Gastric pouch creation with bypass of the remaining stomach and first segment of small intestine Open: 1960s 17.8
Laparoscopic: 1994
Mini-gastric bypass (MGB) Similar to RYGB but with a longer gastric pouch and a longer biliary limb 1997 a

Biliopancreatic diversion (BPD) and BPD: Distal gastrectomy (later: vertical sleeve gastrectomy) with creation of a gastrointestinal BPD: 1979 0.7
duodenal switch (DS); (BPD/DS) anastomosis involving a biliopancreatic bypass DS: BPD modification involving vertical gastrectomy, DS: 1986
some duodenal preservation, and duodenal-intestinal anastomosis involving biliopancreatic bypass
Vertical banded gastroplasty (VBG) Partition of the stomach using staples and placement of a polypropylene mesh band or ring around the 1982 a
outlet of the pouch
Gastric banding (GB) and laparoscopic Gastric partitioning with a ring to create a small upper pouch and the rest of the stomach. GB: 1978 2.77
adjustable gastric banding (LAGB) Later modified to an inflatable balloon ring LAGB: 1986
Sleeve gastrectomy (SG) Resection of 80% of the stomach leaving a tube-shaped gastric pouch. Open: 1988 59.39
Laparoscopic: 1999

a
All other procedures comprise under 2.5% of total cases

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Table 2

Summary of studies assessing the impact of bariatric surgery on control of diabetes

Date Reference: first Study design Surgical patients Control Remission rate: surgical group Remission Average Remission definition
author patients rate: control follow-up
Affinati et al.

group (years)
2010 Poumaras [41] Cohort study 109 RYGB – 72% RYGB – 2–3 FBG< 126 mg/dl, 2 h. OGTT < 200
107 LAGB 17% LAGB mg/dL, Ale < 6.0% w/o meds
2012 Mingrone [44•] RCT 20 RYGB 20 75% RYGB 0% 2 a
20 BPD 95% BPD ADA definition

2013 Arterbum [43•] Retrospective cohort 4434 RYGB – 37.1% 1 year – 3.1 ADA Definition
study 63.3% 3 years
68.2% 5 years
2013 Ikramuddin [45] RCT 60 RYGB 60 44% 9% 1 Ale < 6.0% (secondary outcome)
2013 Liang [46] RCT 31 RYGB b 90% c 0% 1 Off diabetes medications
36 + 34
2014 Halperin [47] RCT 19 RYGB 19 58% 16% 1 Ale < 6.5% off meds
2014 Sjostrom [48] Cohort study 55 RYGB 260 30.4% (composite) 6.5% 15 FBG <110 mg/dL and no meds
61 LAGB
227 SG
2015 Courcoulas [49•] RCT 18 RYGB 14 40% RYGB 0% 3 ADA Definition
20 LAGB 29% LAGB
2015 Ding [50] RCT 23 LAGB 22 33% 23% 1 Ale < 6.5% on or off meds
2015 Mingrone [51•] RCT 20 RYGB 20 37% RYGB 0% 5 ADA Definition
20 BPD 63% BPD
2016 Cummings [52•] RCT 15 RYGB 17 60% 5.9% 1 Ale < 6.0%, off all meds
2017 Schauer [53•] RCT 49 RYGB 38 29% RYGB 5% 5 Ale < 6.0%
47 SG 23% SG
2018 Courcoulas [54] Observational 1738 RYGB – 60.2% RYGB – 7 ADA Definition
Cohort 610 LAGB 20% LAGB

Curr Diab Rep. Author manuscript; available in PMC 2020 September 29.
2018 Ikramuddin [55] RCT 57 RYGB 56 7% 0% 5 Ale < 6.0% off meds (secondary
outcome)
2018 Jacobsen [56] Registry based 855 RYGB 956 57.5% (composite) 14.8% 7.8 No diabetes drugs dispensed
cohort study 69 SG
2018 Lager [57] Retrospective cohort 380 RYGB – 32.1% RYGB – 4 Ale < 6.5% off meds
study 334 SG 22.0% SG
2018 Salminen [58] RCT 52 SG – 12% SG – 5 ADA Definition (secondary
49 RYGB 25% RYGB endpoint)
2018 Simonson [59] RCT 19 RYGB 19 42% 0% 3 Ale <6.5% and FBG <126 mg/dL
on or off meds
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Date Reference: first Study design Surgical patients Control Remission rate: surgical group Remission Average Remission definition
author patients rate: control follow-up
group (years)
2019 Madsen [60] population based 1111 RYGB 1074 74% 1 year – 5 Ale < 6.5% off meds or Ale < 6.0%
cohort 54% 5 years on metformin monotherapy
Affinati et al.

a
ADA definition: normal fasting blood glucose levels and/or HgbA1c without the use of anti-diabetes medications for at least 1 year
b
Usual medical care plus exenatide
b
Diabetes duration of > 10 years was an exclusion criterion

RCT randomized control trial, RYGB Roux-en-Y gastric bypass, LAGB laparoscopic adjustable gastric banding, BPD biliopancreatic diversion, SG sleeve gastrectomy, ADA American Diabetes
Association, FBG Fasting blood glucose, OGTT oral glucose tolerance test

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