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Sleeve gastrectomy (SG) is a commonly performed bariatric procedure. Weight regain following SG is a significant issue. Yet the defining, reporting and understanding of this phenomenon remains largely neglected. Systematic review was performed to locate articles reporting the definition, rate and/or cause of weight regain in patients at least 2 years post-SG. A range of definitions employed to describe weight regain were identified in the literature. Rates of regain ranged from 5.7 % at 2 years to 75.6 % at 6 years. Proposed causes of weight regain included initial sleeve size, sleeve dilation, increased ghrelin levels, inadequate follow-up support and maladaptive lifestyle behaviours. Bariatric literature would benefit from standardising definitions used to report weight regain and its rate in clinical series. Larger prospective studies are required to further understand mechanisms of weight regain following SG.

Inflammation, oxidative stress and dysregulation of adipokines are thought to be pathophysiological mechanisms linking obesity to the development of insulin resistance and atherosclerosis. In adults, bariatric surgery reduces inflammation and oxidative stress, and beneficially changes the levels of several adipokines, but little is known about the postsurgical changes among adolescents. In two separate longitudinal cohorts we evaluated change from baseline of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), monocyte chemo-attractant protein-1 (MCP-1), oxidized low-density lipoprotein cholesterol (oxLDL), adiponectin, leptin and resistin up to 12 months following elective laparoscopic Roux-en-Y gastric bypass (RYGB) or vertical sleeve gastrectomy (VSG) surgery in adolescents with severe obesity. In cohort 1, which consisted of 39 adolescents (mean age 16.5±1.6 years; 29 females) undergoing either RYGB or VSG, IL-6 (baseline: 2.3±3.4 pg ml(-1) vs 12 months: 0.8±0.6 pg ml(-1), P<0.01), leptin (baseline: 178±224 ng ml(-1) vs 12 months: 41.4±31.9 ng ml(-1), P<0.001) and oxLDL (baseline: 41.6±11.6 U l(-1) vs 12 months: 35.5±11.1 U l(-1), P=0.001) significantly decreased and adiponectin significantly increased (baseline: 5.4±2.4 μg ml(-1) vs 12 months: 13.5±8.9 μg ml(-1), P<0.001). In cohort 2, which consisted of 13 adolescents (mean age 16.5±1.6 years; 10 females) undergoing RYGB, results were similar: IL-6 (baseline: 1.7±0.9 pg ml(-1) vs 12 months: 0.4±0.9 pg ml(-1), P<0.05) and leptin (baseline: 92.9±31.3 ng ml(-1) vs 12 months: 37.3±33.4 ng ml(-1), P<0.001) significantly decreased and adiponectin significantly increased (baseline: 6.1±2.9 μg ml(-1) vs 12 months: 15.4±8.0 μg ml(-1), P<0.001). When the cohorts were combined to evaluate changes at 12 months, oxLDL also significantly decreased (baseline: 39.8±16.7 U l(-1) vs 12 months: 32.7±11.9 U l(-1), P=0.03). Bariatric surgery produced robust improvements in markers of inflammation, oxidative stress and several adipokines among adolescents with severe obesity, suggesting potential reductions in risk for type 2 diabetes and cardiovascular disease.

The clinical efficacy of bariatric surgery has encouraged the scientific investigation of the gut as a major endocrine organ. Manipulation of gastrointestinal anatomy through surgery has been shown to profoundly affect the physiological and metabolic processes that control body weight and glycaemia. The most popular bariatric surgical procedures are gastric bypass, adjustable gastric banding and vertical sleeve gastrectomy. Even though these procedures were designed with the aim of causing restriction of food intake and nutrient malabsorption, evidence suggests that their contributions to weight loss are minimal. Instead, these interventions reduce body weight by decreasing hunger, increasing satiation during a meal, changing food preferences and energy expenditure. In this Review, we have explored these mechanisms as well as their mediators. The hope is that that their in-depth investigation will enable the optimization and individualization of surgical techniques, the development of equally effective but safer nonsurgical weight-loss interventions, and even the understanding of the pathophysiology of obesity itself.

This systematic review and meta-analysis aims to establish the effects of bariatric surgery on male sex hormones, sperm parameters, and sexual function. We searched MEDLINE, EMBASE, Web of Science, and Scopus from database inception through June 2018. Articles were eligible for inclusion if they examined the effect of bariatric surgery on male sex hormones and sperm parameters in patients with obesity. Primary outcomes of interest were sex hormones and sperm quality. Secondary outcome was sexual function (International Index of Erectile Function (IIEF) score). Pooled estimates were calculated using random effects meta-analysis. A total of 28 cohort studies with 1022 patients were identified from 3896 potentially relevant citations. Both free and calculated testosterone levels were significantly increased after bariatric surgery (mean difference (MD) − 7.47 nM, 95% CI − 8.62 to − 6.31, p  < 0.001 and MD − 0.05 nM, 95% CI − 0.07 to − 0.02, p  < 0.001, respectively). Consistent with the increase in testosterone, LH, FSH, and SHBG levels were also significantly increased after surgery. In contrast, free and total estradiol and prolactin levels were significantly decreased after bariatric surgery. From studies that reported the IIEF score, bariatric surgery led to a significant increase in erectile function after surgery (MD − 0.46, 95% CI − 0.89 to − 0.02, p  = 0.04). However, bariatric surgery did not affect sperm quality, DHEA, androstenedione, and inhibin B levels. Sustained weight-loss induced by bariatric surgery had a significant effect on increasing male sex hormones and decreasing female sex hormones in male patients with obesity. However, sperm quality and function were not improved after surgery.

BackgroundThe pathogenesis of asthma in obese subjects is poorly understood and has been described as a specific phenotype in these patients. Weight loss improves asthma control and lung function. Whether this improvement is the result of better mechanical properties of the airways or decreased systemic and bronchial inflammation remains unclear.MethodsA longitudinal study in obese patients with asthma (bariatric surgery and asthma group (BS+A), n=27) and obese control (bariatric surgery without asthma group (BS−A), n=39) subjects undergoing bariatric surgery, and obese patients with asthma without intervention (no bariatric surgery and asthma group (NBS+A), n=12). Lung function, asthma control, cellular infiltrates in bronchial biopsies and circulating markers of systemic inflammation were measured during follow up at 3, 6 and 12 months.ResultsBariatric surgery resulted in a profound weight loss at 12 months. In the BS+A group as well as the BS−A group FEV1, functional residual capacity, total lung capacity improved, whereas FEV1/FVC only improved in the BS−A group. In addition, Asthma Control Questionnaire (ACQ), Asthma Quality of Life Questionnaire, inhaled corticosteroid use and PD20 improved in BS+A, whereas in the NBS+A group only ACQ improved. Small airway function R5–R20 improved in both surgery groups, however the change in the BS+A group was greater, resulting in a comparable R5–R20 between BS+A and BS−A at 12-month follow-up. Besides improvement of systemic inflammation (high sensitivity C-reactive protein, adiponectin and leptin) after BS, only a decrease in mast cell numbers was detectable in the BS+A group.ConclusionsBariatric surgery improved small airway function, decreased systemic inflammation and number of mast cells in the airways. These effects could explain the improvement of asthma control, quality of life and lung function. Therefore bariatric surgery, in addition to all other positive effects, also improves asthma in subjects with morbid obesity.Trial registration number3204.

We examined the probability of an obese person attaining normal body weight. We drew a sample of individuals aged 20 years and older from the United Kingdom's Clinical Practice Research Datalink from 2004 to 2014. We analyzed data for 76,704 obese men and 99,791 obese women. We excluded participants who received bariatric surgery. We estimated the probability of attaining normal weight or 5% reduction in body weight. During a maximum of 9 years' follow-up, 1283 men and 2245 women attained normal body weight. In simple obesity (body mass index = 30.0-34.9 kg/m(2)), the annual probability of attaining normal weight was 1 in 210 for men and 1 in 124 for women, increasing to 1 in 1290 for men and 1 in 677 for women with morbid obesity (body mass index = 40.0-44.9 kg/m(2)). The annual probability of achieving a 5% weight reduction was 1 in 8 for men and 1 in 7 for women with morbid obesity. The probability of attaining normal weight or maintaining weight loss is low. Obesity treatment frameworks grounded in community-based weight management programs may be ineffective.

Asprosin is a novel fasting-induced glucogenic and orexigenic protein hormone. The clinical function of asprosin in obesity is currently unknown. This study investigated the association between asprosin abundance and the outcome of bariatric surgery. Patients with body mass index more than 35 kg/m were recruited for the Obesity and Clock for Elegant Aging Registry in 2011-2016. Body weight changes, blood sugar, and asprosin were assessed in 117 patients receiving bariatric surgery and 57 non-obese subjects as normal control. Primary outcomes of excess weight loss percentage at 6 months after bariatric surgery were determined at follow-up. Asprosin levels were significantly higher in obese patients than in non-obese subjects (2360 ± 5094 vs. 307 ± 832 ng/ml, p < 0.0001). Multivariate analyses showed a significant association of asprosin abundance with excess body weight loss percentage at 6 months after surgery (p < 0.0001). After adjusted for age, sex, smoking, HbA1c, cholesterol, and triglyceride, serum asprosin level was the only independent predictor of 6 months excess weight loss percentage after bariatric surgery. Asprosin levels decreased significantly 6 months after bariatric surgery (162.2 ± 169.1 ng/ml). Furthermore, there was no association between asprosin and serum glucose levels in our study. This study provides novel evidence that higher asprosin concentrations before bariatric surgery were associated with the weight reduction magnitude at 6 months after surgery. Further studies are warranted to investigate whether asprosin has direct functions to modulate body weight regulation in humans after bariatric surgery.

Summary The effects of bariatric surgery on skeletal health are poorly understood. We found that bariatric surgery patients are more prone to fracture when compared to the general population. While further studies of fracture risk in this population are needed, bone health should be discussed in bariatric surgery clinics. Introduction Bariatric surgery is an increasingly common treatment for medically complicated obesity. Adverse skeletal changes after bariatric surgery have been reported, but their clinical importance remains unknown. We hypothesized that bariatric surgery patients are at increased risk of fracture. Methods We conducted a historical cohort study of fracture incidence among 258 Olmsted County, Minnesota, residents who underwent a first bariatric surgery in 1985–2004. Relative fracture risk was expressed as standardized incidence ratios (SIRs), while potential risk factors were evaluated by hazard ratios (HR) obtained from a time-to-fracture regression model. Results The mean (±SD) body mass index at bariatric surgery was 49.0 ± 8.4 kg/m 2 , with an average age of 44 ± 10 years and 82 % (212) females. Gastric bypass surgery was performed in 94 % of cases. Median follow-up was 7.7 years (range, 6 days to 25 years), during which 79 subjects experienced 132 fractures. Relative risk for any fracture was increased 2.3-fold (95 % confidence interval (CI), 1.8–2.8) and was elevated for a first fracture at the hip, spine, wrist, or humerus (SIR, 1.9; 95 % CI, 1.1–2.9), as well as for a first fracture at any other site (SIR, 2.5; 95 % CI, 2.0–3.2). Better preoperative activity status was associated with a lower age-adjusted risk (HR, 0.4; 95 % CI, 0.2–0.8) while prior fracture history was not associated with postoperative fracture risk. Conclusions Bariatric surgery, which is accompanied by substantial biochemical, hormonal, and mechanical changes, is associated with an increased risk of fracture.

Roux-en-Y gastric bypass (RYGB) and laparoscopic adjustable gastric banding (LAGB) are anatomically different bariatric operations. RYGB achieves greater weight loss compared with LAGB. Changes in the gut microbiome have been documented after RYGB, but not LAGB, and the microbial contribution to sustainable surgical weight loss warrants further evaluation. We hypothesized that RYGB imposes greater changes on the microbiota and its metabolism than LAGB, and that the altered microbiota may contribute to greater weight loss. Using multi-omic approaches, we analyzed fecal microbial community structure and metabolites of pre-bariatric surgery morbidly obese (PreB-Ob), normal weight (NW), post-RYGB, and post-LAGB participants. RYGB microbiomes were significantly different from those from NW, LAGB and PreB-Ob. Microbiome differences between RYGB and PreB-Ob populations were mirrored in their metabolomes. Diversity was higher in RYGB compared with LAGB, possibly because of an increase in the abundance of facultative anaerobic, bile-tolerant and acid-sensible microorganisms in the former. Possibly because of lower gastric acid exposure, phylotypes from the oral cavity, such as Escherichia, Veillonella and Streptococcus, were in greater abundance in the RYGB group, and their abundances positively correlated with percent excess weight loss. Many of these post-RYGB microorganisms are capable of amino-acid fermentation. Amino-acid and carbohydrate fermentation products-isovalerate, isobutyrate, butyrate and propionate-were prevalent in RYGB participants, but not in LAGB participants. RYGB resulted in greater alteration of the gut microbiome and metabolome than LAGB, and RYGB group exhibited unique microbiome composed of many amino-acid fermenters, compared with nonsurgical controls.

Background Obesity is associated with cardiac dysfunction, atherosclerosis, and increased cardiovascular risk. It can be lead to obesity cardiomyopathy and severe heart failure, which in turn raise morbidity and mortality while carrying a negative impact on quality of life. There is increasing clinical and mechanistic evidence on the metabolic and weight loss effects of bariatric surgery on improving cardiac structure and function in obese patients. Objectives The objective of this study was to quantify the effects of bariatric surgery on cardiac structure and function by appraising cardiac imaging changes before and after metabolic operations. Methods This is a comprehensive systematic review of studies reporting pre-operative and post-operative echocardiographic or magnetic resonance cardiac indices in obese patients undergoing bariatric surgery. Studies were quality scored, and data were meta-analyzed using random effects modeling. Results Bariatric surgery is associated with significant improvements in the weighted incidence of a number of cardiac indices including a decrease in left ventricular mass index (11.2 %, 95 % confidence intervals (CI) 8.2–14.1 %), left ventricular end-diastolic volume (13.28 ml, 95 % CI 5.22–21.34 ml), and left atrium diameter (1.967 mm, 95 % CI 0.980–2.954). There were beneficial increases in left ventricular ejection fraction (1.198 %, 95 %CI −0.050–2.347) and E/A ratio (0.189 %, 95 %CI −0.113–0.265). Conclusions Bariatric surgery offers beneficial cardiac effects on diastolic function, systolic function, and myocardial structure in obese patients. These may derive from surgical modulation of an enterocardiac axis. Future studies must focus on higher evidence levels to better identify the most successful bariatric approaches in preventing and treating the broad spectrum of obesity-associated heart disease while also enhancing treatment strategies in the management of obesity cardiomyopathy.