The recent obesity pandemic has been paralleled by an equally dramatic rise in the prevalence of type 2 diabetes mellitus (T2DM), which is of major concern to healthcare providers globally. The metabolic dysregulation characteristic of T2DM gives rise to a host of macrovascular and microvascular complications, specifically cardiovascular, cerebrovascular and peripheral vascular diseases, as well as retinopathy, nephropathy and neuropathy. The mechanisms underlying development of these complications are multifactorial, and incompletely understood. In addition to the direct injurious effect of hyperglycemia, other purported factors include hypertension, the endocrine activity of adipose tissue, the pro-inflammatory state induced by obesity, and the increased intra-abdominal pressure imposed by central adiposity.

The cost of treating these complications, to patients and society, is exorbitant. The American Diabetes Association’s most recent estimate of the annual economic cost of diabetes was $245 billion (2012 data), a 41 % increase from their previous estimate of $174 billion in 2007 [1]. Much of this (72 %) is accounted for by healthcare costs, the remainder by loss of productivity. With regard to healthcare costs, almost half of this is spent treating microvascular disease complications, particularly diabetic kidney disease(DKD) which accounts for 44 % of cases of renal failure in the US and is the leading indication for renal replacement therapy at present.

Furthermore, data from the Third National Health and Nutrition Examination Survey (NHANES III) in the US highlights the mortality risk associated with diabetic kidney disease (DKD) by demonstrating that there is a 400 % increase in 10-year all-cause mortality for patients with DKD relative to the non-diabetic populations, largely attributable to death from associated cardiovascular disease [2].

Hitherto, clinicians have focused on attaining tight glycemic control through pharmacological interventions to prevent and/or arrest the macrovascular and microvascular complications of T2DM. While this is certainly effective, as evidenced by the intensive treatment arms of the first United Kingdom prospective diabetes study (UKPDS) glycemic control study, the Action in Diabetes and Vascular Disease Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) randomized controlled trial and the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, the benefits are marginal [3–5]. At most, a 33 % reduction in the progression of diabetic retinopathy was observed in the ACCORD trial, and although minor reductions in the incidence and progression of albuminuria were noted in this study, they were counter-intuitively coincident with a higher rate of doubling of serum creatinine in the intensified treatment group. The ADVANCE study reported a 10 % decrease in a composite end-point of macrovascular and microvascular disease that was not significant after adjusting for a 21 % decrease in new or worsening nephropathy, and no significant difference in retinopathy was observed following treatment intensification. Synthesis of data from these and similar studies indicates that a multimodal approach targeting both blood pressure and glycemic control is optimal in relation to providing for an effective reduction in microvascular complications in combination with reductions in all-cause mortality and cardiovascular events, neither of which are well met by individual treatment intensification strategies.

Metabolic (bariatric) surgery has revolutionized the management of severe obesity and obesity-related comorbidities in recent years. In addition to substantial weight loss, it leads to dramatic improvements in glycemic control, insulin sensitivity, and cardiovascular disease risk. To date, 11 randomized controlled trials have directly compared medical versus surgical treatment for T2DM [6]. The first of these, by Dixon et al. compared the two year outcomes of conventional medical treatment with gastric banding for the management of T2DM, in 60 obese patients [7]. More recently, Schauer et al. and Mingrone et al. evaluated the 12, 24 and 36 month effects of bariatric surgery (gastric bypass, sleeve gastrectomy, or biliopancreatic diversion) compared to intensive medical therapy on diabetes management [8–10]. All 3 groups demonstrated that weight loss surgery was far more effective than medical therapy at inducing remission or improvement of diabetes. Meta-analysis of the data from the 11 RCTs comparing multimodal medical therapy with bariatric surgery for management of T2DM indicates that weight loss was significantly greater in the surgical groups and bariatric surgery patients had a higher remission rate of T2DM (relative risk 22.1 (3.2–154.3)) and metabolic syndrome (relative risk 2.4 (1.6–3.6)), greater improvements in quality of life and reductions in medicine use. Other notable benefits in the surgical arms of these trials included significant decrease in plasma triglyceride concentrations, and increase in high density lipoprotein cholesterol concentrations [6]. Although not included in this meta-analysis because it was not a randomized trial, the noteworthy Swedish Obese Subjects (SOS) case-control study demonstrated a hazard ratio of 0.17 for diabetes incidence following assorted bariatric surgical interventions illustrating how effectively bariatric surgery reduces progression from the pre-diabetic state [11]. The SOS studies have also shown that bariatric surgery is associated with a decreased incidence of diabetic microvascular complications (HR 0.44; 95 % CI, 0.34–0.56; p < 0.001) and macrovascular complications (HR 0.68; 95 % CI, 0.54–0.85; p < .001) [12]. These benefits are obviously not without risk. Whilst there were no deaths reported after bariatric surgery in any of the RCTs included in this meta-analysis, common adverse events after bariatric surgery were iron deficiency anemia (15 % of individuals undergoing malabsorptive bariatric surgery) and reoperations (8 %).