Sudden death after open gastric bypass surgery

Purpose: Gastric bypass surgery has become a relatively low-risk bariatric surgical intervention in a high-risk patient population (Nguyen et al., Arch Surg, 141:445-449, 2006; Buchwald et al. JAMA, 13:1724-1737, 2004). Surgical interventions in patients suffering from morbid obesity are typically associated with excess morbidity (Parikh et al., Am Surg, 73:959-962, 2007). Though overall mortality after bariatric surgery is <1% is low (Mason et al., Obes Surg, 17:9-14, 2007), some surgical complications such as anastomotic leaks, staple line disruption and bowel obstruction may still impact on postoperative outcome (Parikh et al., Am Surg, 73:959-962, 2007; Mason et al., Obes Surg, 17:9-14, 2007). Early symptoms are often missed, as clinical presentation may be discreet, inexistent or falsely attributed to obesity. Methods: This case report refers to a patient in whom discomfort and agitation associated with a rise in temperature heralded a fulminant septic shock syndrome precipitating his death. Literature on early complications and management after gastric bypass is reviewed. Conclusion: A high level of suspicion should be present in the case of an unexpected postoperative deterioration of the patient's general condition. Time to treat may be very short (Mason et al., Obes Surg, 17:9-14, 2007). Computed tomography is mandatory to rule out pulmonary embolism and bypass obstructio

Green tea extract enhances parieto-frontal connectivity during working memory processing

Rationale: It has been proposed that green tea extract may have a beneficial impact on cognitive functioning, suggesting promising clinical implications. However, the neural mechanisms underlying this putative cognitive enhancing effect of green tea extract still remain unknown. Objectives: This study investigates whether the intake of green tea extract modulates effective brain connectivity during working memory processing and whether connectivity parameters are related to task performance. Material and methods: Using a double-blind, counterbalanced, within-subject design, 12 healthy volunteers received a milk whey-based soft drink containing 27.5g of green tea extract or a milk whey-based soft drink without green tea as control substance while undergoing functional magnetic resonance imaging. Working memory effect on effective connectivity between frontal and parietal brain regions was evaluated using dynamic causal modeling. Results: Green tea extract increased the working memory induced modulation of connectivity from the right superior parietal lobule to the middle frontal gyrus. Notably, the magnitude of green tea induced increase in parieto-frontal connectivity positively correlated with improvement in task performance. Conclusions: Our findings provide first evidence for the putative beneficial effect of green tea on cognitive functioning, in particular, on working memory processing at the neural system level by suggesting changes in short-term plasticity of parieto-frontal brain connections. Modeling effective connectivity among frontal and parietal brain regions during working memory processing might help to assess the efficacy of green tea for the treatment of cognitive impairments in psychiatric disorders such as dementia

Validation of the individualized metabolic surgery score for bariatric procedure selection in the merged data of two randomized clinical trials (SLEEVEPASS and SM-BOSS).

Background: LSG and LRYGB are globally the most common bariatric procedures. IMS score categorizes T2D severity (mild, moderate, and severe) based on 4 independent preoperative predictors of long-term remission as follows: T2D duration, number of diabetes medications, insulin use, and glycemic control. IMS score has not been validated in a randomized patient cohort.Objectives: To assess the feasibility of individualized metabolic surgery (IMS) score in facilitating procedure selection between laparoscopic sleeve gastrectomy (LSG) and laparoscopic Roux-en-Y gastric bypass (LRYGB) for patients with severe obesity and type 2 diabetes (T2D).Setting: Merged individual patient-level 5-year data of 2 large randomized clinical trials (SLEEVEPASS and SM-BOSS [Swiss Multicenter Bypass or Sleeve Study]).Methods: IMS score was calculated for study patients and its performance was analyzed.Results: One hundred thirty-nine out of 155 patients with T2D had available preoperative data to calculate IMS score as follows: mild stage (n = 41/139), moderate stage (n = 77/139), severe stage (n = 21/139). At 5 years, 135 (87.1%, 67 LSG/68 LRYGB) were available for follow-up and 121 patients had both pre- and postoperative data. Diabetes remission rates according to preoperative IMS score were as follows: mild stage 87.5% (n = 14/16) after LSG and 85.7% (n = 18/21) after LRYGB (P = .999), moderate stage 42.9% (n = 15/35) and 45.2% (n = 14/31) (P = .999), and severe stage 18.2% (n = 2/11) and 0% (n = 0/7) (P = .497), respectively. The T2D remission rate varied significantly between the stages as follows: mild versus moderate odds ratio (OR) 8.3 (95% CI, 2.8-24.0; P Conclusions: In our study, remission rates of T2D were not statistically different after LSG and LRYGB among all patients and among patients with mild, moderate, and severe diabetes stratified by the IMS score. However, the study may be underpowered to detect differences due to small number of patients in each subgroup. IMS score seemed to be useful in predicting long-term T2D remission after bariatric surgery.</p

Effect of the natural sweetener xylitol on gut hormone secretion and gastric emptying in humans:A pilot dose-ranging study

Sugar consumption is associated with a whole range of negative health effects and should be reduced and the natural sweetener xylitol might be helpful in achieving this goal. The present study was conducted as a randomized, placebo-controlled, double-blind, cross-over trial. Twelve healthy, lean volunteers received intragastric solutions with 7, 17 or 35 g xylitol or tap water on four separate days. We examined effects on: gut hormones, glucose, insulin, glucagon, uric acid, lipid profile, as well as gastric emptying rates, appetite-related sensations and gastrointestinal symptoms. We found: (i) a dose-dependent stimulation of cholecystokinin (CCK), active glucagon-like peptide-1 (aGLP-1), peptide tyrosine tyrosine (PYY)-release, and decelerated gastric emptying rates, (ii) a dose-dependent increase in blood glucose and insulin, (iii) no effect on motilin, glucagon, or glucose-dependent insulinotropic peptide (GIP)-release, (iv) no effect on blood lipids, but a rise in uric acid, and (v) increased bowel sounds as only side effects. In conclusion, low doses of xylitol stimulate the secretion of gut hormones and induce a deceleration in gastric emptying rates. There is no effect on blood lipids and only little effect on plasma glucose and insulin. This combination of properties (low-glycemic sweetener which stimulates satiation hormone release) makes xylitol an attractive candidate for sugar replacement

Diet-induced loss of adipose Hexokinase 2 triggers hyperglycemia

Chronically high blood glucose (hyperglycemia) leads to diabetes, fatty liver disease, and cardiovascular disease. Obesity is a major risk factor for hyperglycemia, but the underlying mechanism is unknown. Here we show that a high fat diet (HFD) in mice causes early loss of expression of the glycolytic enzyme Hexokinase 2 (HK2) specifically in adipose tissue. Adipose-specific knockout of Hk2 caused enhanced gluconeogenesis and lipogenesis in liver, a condition known as selective insulin resistance, leading to glucose intolerance. Furthermore, we observed reduced hexokinase activity in adipose tissue of obese and diabetic patients, and identified a loss-of-function mutation in the hk2 gene of naturally hyperglycemic Mexican cavefish. Mechanistically, HFD in mice led to loss of HK2 by inhibiting translation of Hk2 mRNA. Our findings identify adipose HK2 as a critical mediator of systemic glucose homeostasis, and suggest that obesity-induced loss of adipose HK2 is an evolutionarily conserved, non-cell-autonomous mechanism for the development of hyperglycemia