Long-term outcome after biliopancreatic diversion with duodenal switch: a single-center experience with up to 20 years follow-up.

BACKGROUND: Biliopancreatic diversion with duodenal switch (BPD/DS) is the most effective standard bariatric procedure in terms of weight loss and remission of co-morbidities but carries the risk of severe long-term side effects. OBJECTIVE: The aim of this study was to analyze the long-term effects of BPD/DS in terms of morbidity, weight loss, remission of associated medical problems, deficiencies, and reoperations. SETTING: Academic teaching hospital, Switzerland. METHODS: This is a retrospective, single-center study of prospectively collected data of all patients who underwent BPD/DS from 1999 to 2011 with a minimal follow-up (FU) of 10 years. RESULTS: A total of 116 patients (83.6% female) underwent BPD/DS with a mean initial body mass index (BMI) of 47 ± 6.5 kg/m2. Of these, 68% of the procedures were performed in open technique and 32% laparoscopically. The majority (76.7%) of patients had laparoscopic adjustable gastric banding before BPD/DS. The mean FU time was 14 ± 4.4 years and the FU rate at 5, 10, and 14 years was 95.6% (n = 108), 90% (n = 98), and 75.3% (n = 70), respectively. The mean excess BMI loss at 5, 10, and 14 years was 78% ± 24.1%, 76.5% ± 26.7%, and 77.8% ± 33.8%, respectively. Complete (n = 22) or partial remission (n = 4) of type 2 diabetes was observed in 92.8% of patients. Forty reoperations were necessary in 34 patients (29.3%) because of malnutrition or refractory diarrhea (n = 13), insufficient weight loss or weight rebound (n = 7), reflux or stenosis (n = 10), and various/combined indications (n = 10). The mean time to reoperation was 7.7 ± 5 years. There were no procedure-related deaths in the short or long term. CONCLUSIONS: BPD/DS offers sustainable long-term weight loss but is associated with important side effects that may be acceptable in selected patients with a high initial BMI (>50 kg/m2) and/or for nonresponders after primary restrictive procedures. Regular FU is necessary to detect and treat malnutrition and vitamin deficiencies.

Impact of laparoscopic Roux-en-Y gastric bypass and sleeve gastrectomy on gut microbiota: a metagenomic comparative analysis.

BACKGROUND: Bariatric surgery is an effective therapeutic procedure for morbidly obese patients. The 2 most common interventions are sleeve gastrectomy (SG) and laparoscopic Roux-en-Y gastric bypass (LRYGB). OBJECTIVES: The aim of this study was to compare microbiome long-term microbiome after SG and LRYGB surgery in obese patients. SETTING: University Hospital, France; University Hospital, United States; and University Hospital, Switzerland. METHODS: Eighty-nine and 108 patients who underwent SG and LRYGB, respectively, were recruited. Stools were collected before and 6 months after surgery. Microbial DNA was analyzed with shotgun metagenomic sequencing (SOLiD 5500 xl Wildfire). MSPminer, a novel innovative tool to characterize new in silico biological entities, was used to identify 715 Metagenomic Species Pan-genome. One hundred forty-eight functional modules were analyzed using GOmixer and KEGG database. RESULTS: Both interventions resulted in a similar increase of Shannon's diversity index and gene richness of gut microbiota, in parallel with weight loss, but the changes of microbial composition were different. LRYGB led to higher relative abundance of aero-tolerant bacteria, such as Escherichia coli and buccal species, such as Streptococcus and Veillonella spp. In contrast, anaerobes, such as Clostridium, were more abundant after SG, suggesting better conservation of anaerobic conditions in the gut. Enrichment of Akkermansia muciniphila was also observed after both surgeries. Function-level changes included higher potential for bacterial use of supplements, such as vitamin B12, B1, and iron upon LRYGB. CONCLUSION: Microbiota changes after bariatric surgery depend on the nature of the intervention. LRYGB induces greater taxonomic and functional changes in gut microbiota than SG. Possible long-term health consequences of these alterations remain to be established.

Effect of cocoa on the brain and gut in healthy subjects: a randomised controlled trial.

Dark chocolate is claimed to have effects on gastrointestinal function and to improve well-being. This randomised controlled study tested the hypothesis that cocoa slows gastric emptying and intestinal transit. Functional brain imaging identified central effects of cocoa on cortical activity. Healthy volunteers (HV) ingested 100 g dark (72 % cocoa) or white (0 % cocoa) chocolate for 5 d, in randomised order. Participants recorded abdominal symptoms and stool consistency by the Bristol Stool Score (BSS). Gastric emptying (GE) and intestinal and colonic transit time were assessed by scintigraphy and marker studies, respectively. Combined positron emission tomography-computed tomography (PET-CT) imaging assessed regional brain activity. A total of sixteen HV (seven females and nine males) completed the studies (mean age 34 (21-58) years, BMI 22·8 (18·5-26·0) kg/m2). Dark chocolate had no effect on upper gastrointestinal function (GE half-time 82 (75-120) v. 83 (60-120) min; P=0·937); however, stool consistency was increased (BSS 3 (3-5) v. 4 (4-6); P=0·011) and there was a trend to slower colonic transit (17 (13-26) v. 21 (15-47) h; P=0·075). PET-CT imaging showed increased [18F]fluorodeoxyglucose (FDG) in the visual cortex, with increased FDG uptake also in somatosensory, motor and pre-frontal cortices (P<0·001). In conclusion, dark chocolate with a high cocoa content has effects on colonic and cerebral function in HV. Future research will assess its effects in patients with functional gastrointestinal diseases with disturbed bowel function and psychological complaints.

Insulin resistance causes inflammation in adipose tissue.

Obesity is a major risk factor for insulin resistance and type 2 diabetes. In adipose tissue, obesity-mediated insulin resistance correlates with the accumulation of proinflammatory macrophages and inflammation. However, the causal relationship of these events is unclear. Here, we report that obesity-induced insulin resistance in mice precedes macrophage accumulation and inflammation in adipose tissue. Using a mouse model that combines genetically induced, adipose-specific insulin resistance (mTORC2-knockout) and diet-induced obesity, we found that insulin resistance causes local accumulation of proinflammatory macrophages. Mechanistically, insulin resistance in adipocytes results in production of the chemokine monocyte chemoattractant protein 1 (MCP1), which recruits monocytes and activates proinflammatory macrophages. Finally, insulin resistance (high homeostatic model assessment of insulin resistance [HOMA-IR]) correlated with reduced insulin/mTORC2 signaling and elevated MCP1 production in visceral adipose tissue from obese human subjects. Our findings suggest that insulin resistance in adipose tissue leads to inflammation rather than vice versa.

Metabolic and hormonal changes after laparoscopic Roux-en-Y gastric bypass and sleeve gastrectomy: a randomized, prospective trial.

BACKGROUND: The mechanisms of amelioration of glycemic control early after laparoscopic Roux-en-Y gastric bypass (LRYGB) or laparoscopic sleeve gastrectomy (LSG) are not fully understood. METHODS: In this prospective, randomized 1-year trial, outcomes of LRYGB and LSG patients were compared, focusing on possibly responsible mechanisms. Twelve patients were randomized to LRYGB and 11 to LSG. These non-diabetic patients were investigated before and 1 week, 3 months, and 12 months after surgery. A standard test meal was given after an overnight fast, and blood samples were collected before, during, and after food intake for hormone profiles (cholecystokinin (CCK), ghrelin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY)). RESULTS: In both groups, body weight and BMI decreased markedly and comparably leading to an identical improvement of abnormal glycemic control (HOMA index). Post-surgery, patients had markedly increased postprandial plasma GLP-1 and PYY levels (p < 0.05) with ensuing improvement in glucose homeostasis. At 12 months, LRYGB ghrelin levels approached preoperative values. The postprandial, physiologic fluctuation returned, however, while LSG ghrelin levels were still markedly attenuated. One year postoperatively, CCK concentrations after test meals increased less in the LRYGB group than they did in the LSG group, with the latter showing significantly higher maximal CCK concentrations (p < 0.012 vs. LRYGB). CONCLUSIONS: Bypassing the foregut is not the only mechanism responsible for improved glucose homeostasis. The balance between foregut (ghrelin, CCK) and hindgut (GLP-1, PYY) hormones is a key to understanding the underlying mechanisms.

Effects of postbariatric surgery weight loss on adipokines and metabolic parameters: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy--a prospective randomized trial.

BACKGROUND: Laparoscopic Roux-en-Y gastric bypass (LRYGB) and laparoscopic sleeve gastrectomy (LSG) lead to rapid improvement in insulin sensitivity even before weight loss occurs. Adipokines are closely linked to obesity and insulin resistance. To date, it is unclear whether the different anatomic changes of the various bariatric procedures have different effects on hormones of adipocyte origin. In the present prospective, randomized study, we compared the 1-year follow-up results of LRYGB and LSG concerning weight loss, metabolic control, and fasting adipokine levels. METHODS: Of 23 nondiabetic morbidly obese patients, 12 were randomized to LRYGB and 11 to LSG. The patients were investigated before and 1 week, 3 months, and 12 months after surgery. The fasting levels of glucose, insulin, lipids, and adipokines (leptin, adiponectin, and fibroblast growth factor-21) were analyzed. RESULTS: The body weight decreased markedly (P <.001) after either procedure (percentage of weight loss 16.4% ± 1.3%, 24.8% ± 1.7%, and 34.5% ± 2.7% after LRYGB and 13.1% ± 1.1%, 20.7% ± 1.5%, and 27.9% ± 2.6% after LSG at 2, 6, and 12 mo, respectively). The Homeostasis Model Assessment Index declined from 8.0 ± 1.5 preoperatively to 2.9 ± .2 at 12 months after LRYGB and from 7.5 ± 1.7 preoperatively to 3.3 ± .3 at 12 months after LSG. The lipid profiles were normalized. The concentrations of circulating leptin levels decreased by almost 50% as early as 1 week postoperatively and continued to decrease until 12 months postoperatively. Adiponectin increased progressively. The fibroblast growth factor-21 levels did not change over time. No difference was found between the LRYGB and LSG groups. CONCLUSION: Both procedures led to significant weight loss associated with the resolution of the metabolic syndrome. The serum leptin levels decreased and adiponectin increased with weight loss, paralleled by improved insulin sensitivity.