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).

BACKGROUND: Laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (LRYGB) are both effective surgical procedures to achieve weight reduction in patients with obesity. The trial objective was to merge individual-patient data from two RCTs to compare outcomes after LSG and LRYGB. METHODS: Five-year outcomes of the Finnish SLEEVEPASS and Swiss SM-BOSS RCTs comparing LSG with LRYGB were analysed. Both original trials were designed to evaluate weight loss. Additional patient-level data on type 2 diabetes (T2DM), obstructive sleep apnoea, and complications were retrieved. The primary outcome was percentage excess BMI loss (%EBMIL). Secondary predefined outcomes in both trials included total weight loss, remission of co-morbidities, improvement in quality of life (QoL), and overall morbidity. RESULTS: At baseline, 228 LSG and 229 LRYGB procedures were performed. Five-year follow-up was available for 199 of 228 patients (87.3 per cent) after LSG and 199 of 229 (87.1 per cent) after LRYGB. Model-based mean estimate of %EBMIL was 7.0 (95 per cent c.i. 3.5 to 10.5) percentage points better after LRYGB than after LSG  (62.7 versus 55.5 per cent respectively; P < 0.001). There was no difference in remission of T2DM, obstructive sleep apnoea or QoL improvement; remission for hypertension was better after LRYGB compared with LSG (60.3 versus 44.9 per cent; P = 0.049). The complication rate was higher after LRYGB than LSG (37.2 versus 22.5 per cent; P = 0.001), but there was no difference in mean Comprehensive Complication Index value (30.6 versus 31.0 points; P = 0.859). CONCLUSION: Although LRYGB induced greater weight loss and better amelioration of hypertension than LSG, there was no difference in remission of T2DM, obstructive sleep apnoea, or QoL at 5 years. There were more complications after LRYGB, but the individual burden for patients with complications was similar after both operations.

Functional roles of low calorie sweeteners on gut function.

This short review summarizes the effects of low calorie sweeteners (fructose, non-nutritive low calorie sweeteners) on gut functions focusing on the gut sweet taste receptor system. The effects of these molecules on secretion of gut peptides associated with glycemic homeostasis and appetite regulation is reviewed as well as effects on gastric emptying and glucose absorption.

Gut sweet taste receptors and their role in metabolism.

Obesity is caused by an imbalance between food intake and energy expenditure. In recent decades the gastrointestinal tract has received growing attention as a control parameter for the regulation of appetite and food intake, however regulatory circuits and their interactions are complex. The basic understanding on the role of the gut starts with the notion 'we are what we eat'. Food enters the gastrointestinal tract, which then triggers specific mechanisms or a sensing machinery that respond to specific components of food. Enteroendocrine cells in the small intestine are the anatomical basis for the sensing machinery, which act as neural triggers or as intestinal satiation peptide-secreting cells. These cells express chemosensory receptors that respond to luminal stimuli. The understanding of each gastrointestinal mechanism that might be involved in the process of eating provides a basis for the assessment of the potential of the gastrointestinal tract in the fight against obesity. This review discusses the function of the gut sweet taste receptor T1R2/T1R3 in sensing sweet compounds, as well as its role in gastrointestinal peptide secretion and glucose metabolism.

Effects of chenodeoxycholic acid on the secretion of gut peptides and fibroblast growth factors in healthy humans.

CONTEXT: Recent evidence suggests bile acids (BAs) are involved in the glycemic control via TGR5 activation with the subsequent release of gut peptides and farnesoid X receptor activation with ensuing release of fibroblast growth factors (FGFs). OBJECTIVE: We hypothesized that intraduodenal infusions of chenodeoxycholic acid (CDCA) would stimulate FGF and gut peptide secretion, thereby positively influencing glucose homeostasis. DESIGN, SETTING, PARTICIPANTS, AND INTERVENTION: This randomized, double-blind, placebo-controlled, crossover trial included 12 healthy volunteers who received intraduodenal infusions (2.0 mL/min for 180 minutes) of saline, CDCA (5 or 15 mmol/L), and a fatty acid (sodium oleate), either alone or with 5 mmol/L CDCA. After 60 minutes, an oral glucose tolerance test (oGTT) was performed. MAIN OUTCOME MEASURES: Plasma levels of glucagon-like peptide-1 (GLP-1), peptide tyrosine tyrosine, cholecystokinin (CCK), total BAs, FGF19, FGF21, C-peptide, insulin, glucose, and glucagon were measured. RESULTS: Within the first 60 minutes, high-concentration CDCA induced a small but significant increase in GLP-1 and CCK secretion (P = .016 and P =.011), whereas plasma C-peptide, insulin, and glucose were not affected. Attenuated C-peptide and insulin release was observed after the oGTT with 15 mmol/L CDCA (P = .013 and P =.011). Plasma BA and FGF19 levels significantly increased after CDCA administration (P = .001 and P < .001). CONCLUSIONS: CDCA modulates GLP-1 and CCK secretion; the effect is small and does not influence glucose levels. The marked increase in plasma BAs and the attenuated insulin release after the oGTT indicate the role of BAs in glycemic control, independent of the incretin axis, and suggest involvement of farnesoid X receptor activation pathways.