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Background: Despite growing evidence that bariatric/metabolic surgery powerfully improves type 2 diabetes (T2D), existing diabetes treatment algorithms do not include surgical options.Aim: The 2nd Diabetes Surgery Summit (DSS-II), an international consensus conference, was convened in collaboration with leading diabetes organizations to develop global guidelines to inform clinicians and policymakers about benefits and limitations of metabolic surgery for T2D.Methods: A multidisciplinary group of 48 international clinicians/scholars (75% nonsurgeons), including representatives of leading diabetes organizations, participated in DSS-II. After evidence appraisal (MEDLINE [1 January 2005-30 September 2015]), three rounds of Delphi-like questionnaires were used to measure consensus for 32 data-based conclusions. These drafts were presented at the combined DSS-II and 3rd World Congress on Interventional Therapies for Type 2 Diabetes (London, U.K., 28-30 September 2015), where they were open to public comment by other professionals and amended face-to-face by the Expert Committee.Results: Given its role in metabolic regulation, the gastrointestinal tract constitutes a meaningful target to manage T2D. Numerous randomized clinical trials, albeit mostly short/midterm, demonstrate that metabolic surgery achieves excellent glycemic control and reduces cardiovascular risk factors. On the basis of such evidence, metabolic surgery should be recommended to treat T2D in patients with class III obesity (BMI ≥40 kg/m(2)) and in those with class II obesity (BMI 35.0-39.9 kg/m(2)) when hyperglycemia is inadequately controlled by lifestyle and optimal medical therapy. Surgery should also be considered for patients with T2D and BMI 30.0-34.9 kg/m(2) if hyperglycemia is inadequately controlled despite optimal treatment with either oral or injectable medications. These BMI thresholds should be reduced by 2.5 kg/m(2) for Asian patients.Conclusions: Although additional studies are needed to further demonstrate long-term benefits, there is sufficient clinical and mechanistic evidence to support inclusion of metabolic surgery among antidiabetes interventions for people with T2D and obesity. To date, the DSS-II guidelines have been formally endorsed by 45 worldwide medical and scientific societies. Health care regulators should introduce appropriate reimbursement policies. [ABSTRACT FROM AUTHOR]

Background: Obesity-related dyslipidaemia comprises hypercholesterolaemia, hypertriglyceridaemia, low HDL-cholesterol and normal to raised LDL-cholesterol levels. 40 % of morbidly obese surgical patients have dyslipidaemia. Roux-en-Y gastric bypass (RYGB) surgery has many beneficial metabolic effects, but the full impact on plasma lipids has not been clearly defined. Methods: A systematic review of electronic databases (Ovid; Medline; PubMed; Embase) between 1960 and March 2012 was performed using search terms including the following: obesity surgery, bariatric surgery, gastric bypass, cholesterol, lipids, triglycerides and non-esterified fatty acids. A total of 2442 manuscripts were screened. Papers with paired plasma lipid levels around RYGB surgery were included. Exclusions included the following: editorials, dual publications, n < 10, resulting in 75 papers of relevance. A meta-analysis was performed of the effect of RYGB surgery upon plasma lipids at different time points up to 4 years following surgery, using a random effects model. Results: Paired data were available for 7815 subjects around RYGB surgery for morbid obesity with a baseline BMI 48 kg/m ( n = 2331). There was a reduction in plasma total cholesterol and LDL-C from 1 month up to 4 years post-RYGB ( p < 0.00001, p < 0.00001). Following RYGB, HDL-C increased from 1 year onwards ( p < 0.00001), and triglyceride levels were reduced postoperatively from 3 months up to 4 years ( p < 0.00001). NEFA levels were increased at 1 month postoperatively ( p = 0.003), but from 3 months onwards did not differ from preoperative levels ( p = 0.07). Conclusions: RYGB surgery reverses the dyslipidaemia of obesity. These findings support the use of RYGB in the management of high cardiovascular risk lipid profiles in morbid obesity. [ABSTRACT FROM AUTHOR]

Hypertriglyceridemia is associated with an increased risk of type 2 diabetes. We aimed to comprehensively examine the effects of hypertriglyceridemia on major glucose homeostatic mechanisms involved in diabetes progression. In this randomized, cross-over, single-blinded study, two dual-labeled, 3-hour oral glucose tolerance tests were performed during 5-hour intravenous infusions of either 20 % Intralipid or saline in 12 healthy subjects (age 27.9 ± 2.6 years, 11 men, BMI 22.6 ± 1.4 kg/m2) to evaluate lipid-induced changes in insulin metabolism and glucose kinetics. Insulin sensitivity, β cell secretory function, and insulin clearance were assessed by modeling glucose, insulin and C-peptide data. Intestinal glucose absorption, endogenous glucose production, and glucose clearance were assessed from glucose tracers. The effect of triglycerides on β-cell secretory function was examined in perifusion experiments in murine pseudoislets and human pancreatic islets. Mild acute hypertriglyceridemia impaired oral glucose tolerance (mean glucose: +0.9 [0.3, 1.5] mmol/L, p = 0.008) and whole-body insulin sensitivity (Matsuda index: −1.67 [−0.50, −2.84], p = 0.009). Post-glucose hyperinsulinemia (mean insulin: +99 [17, 182] pmol/L, p = 0.009) resulted from reduced insulin clearance (−0.16 [−0.32, −0.01] L min−1 m−2, p = 0.04) and enhanced hyperglycemia-induced total insulin secretion (+11.9 [1.1, 22.8] nmol/m2, p = 0.02), which occurred despite a decline in model-derived β cell glucose sensitivity (−41 [−74, −7] pmol min−1 m−2 mmol−1 L, p = 0.04). The analysis of tracer-derived glucose metabolic fluxes during lipid infusion revealed lower glucose clearance (−96 [−152, −41] mL/kg FFM , p = 0.005), increased 2-hour oral glucose absorption (+380 [42, 718] μmol/kg FFM , p = 0.04) and suppressed endogenous glucose production (−448 [−573, −123] μmol/kg FFM , p = 0.005). High-physiologic triglyceride levels increased acute basal insulin secretion in murine pseudoislets (+11 [3, 19] pg/aliquot, p = 0.02) and human pancreatic islets (+286 [59, 512] pg/islet, p = 0.02). Our findings support a critical role for hypertriglyceridemia in the pathogenesis of type 2 diabetes in otherwise healthy individuals and dissect the glucose homeostatic mechanisms involved, encompassing insulin sensitivity, β cell function and oral glucose absorption. [Display omitted] • Mild acute hypertriglyceridemia has marked negative effects on oral glucose tolerance. • Mechanisms include whole body insulin resistance and faster glucose absorption. • These effects are attenuated by lipid-induced hyperinsulinemia. [ABSTRACT FROM AUTHOR]