Is the Roux Limb a Determinant for Meal Size After Gastric Bypass Surgery?

The Roux-Y gastric bypass (RYGBP) is an effective weight-reducing procedure but the involved mechanisms of action are obscure. The Roux limb is the intestinal segment that following surgery is the primary recipient for food intake. The aims of the study were to explore the mechanosensory and biomechanical properties of the Roux limb and to make correlations with preferred meal size. Ten patients participated and were examined preoperatively, 6 weeks and 1 year after RYGBP. Each subject ingested unrestricted amounts of a standardized meal and the weight of the meal was recorded. On another study day, the Roux limb was subjected to gradual distension by the use of an intraluminal balloon. Luminal volume–pressure relationships and thresholds for induction of sensations were monitored. At 6 weeks and 1 year post surgery, the subjects had reduced their meal sizes by 62% and 41% (medians), respectively, compared to preoperative values. The thresholds for eliciting distension-induced sensations were strongly and negatively correlated to the preferred meal size. Intraluminal pressure during Roux limb distension, both at low and high balloon volumes, correlated negatively to the size of the meal that the patients had chosen to eat. The results suggest that the Roux limb is an important determinant for regulating food intake after Roux-Y bypass bariatric surgery

Obesity: An overview on its current perspectives and treatment options

Obesity is a multi-factorial disorder, which is often associated with many other significant diseases such as diabetes, hypertension and other cardiovascular diseases, osteoarthritis and certain cancers. The management of obesity will therefore require a comprehensive range of strategies focussing on those with existing weight problems and also on those at high risk of developing obesity. Hence, prevention of obesity during childhood should be considered a priority, as there is a risk of persistence to adulthood. This article highlights various preventive aspects and treatment procedures of obesity with special emphasis on the latest research manifolds

Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009

Insulin resistance is a hallmark of type 2 diabetes mellitus and is associated with a metabolic and cardiovascular cluster of disorders (dyslipidaemia, hypertension, obesity [especially visceral], glucose intolerance, endothelial dysfunction), each of which is an independent risk factor for cardiovascular disease (CVD). Multiple prospective studies have documented an association between insulin resistance and accelerated CVD in patients with type 2 diabetes, as well as in non-diabetic individuals. The molecular causes of insulin resistance, i.e. impaired insulin signalling through the phosphoinositol-3 kinase pathway with intact signalling through the mitogen-activated protein kinase pathway, are responsible for the impairment in insulin-stimulated glucose metabolism and contribute to the accelerated rate of CVD in type 2 diabetes patients. The current epidemic of diabetes is being driven by the obesity epidemic, which represents a state of tissue fat overload. Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes. Treatment with thiazolidinediones mobilises fat out of tissues, leading to enhanced insulin sensitivity, improved beta cell function and decreased atherogenesis. Insulin resistance and lipotoxicity represent the missing links (beyond the classical cardiovascular risk factors) that help explain the accelerated rate of CVD in type 2 diabetic patients

Human gastric B cell responses can be induced by intestinal immunisation

BACKGROUND—In a previous study, we found that oral vaccination induces strong B cell responses in the stomach of Helicobacter pylori infected but not of uninfected individuals. In this study, we have evaluated the possibility of inducing gastric immune responses in H pylori infected volunteers by intestinal and gastric immunisation.
METHODS—H pylori infected subjects were given two doses of an inactivated cholera vaccine, either intestinally via an endoscope approximately 30 cm distal to the pylorus sphincter or intragastrically as small droplets applied directly onto the stomach mucosa. Uninfected individuals received the vaccine by standard oral procedure. Vaccine specific antibody secreting cells in antral and duodenal biopsies were detected by the enzyme linked immunospot assay technique before and seven days after the second immunisation.
RESULTS—Intestinal immunisations resulted in induction of vaccine specific gastric IgA secreting cells in five of eight volunteers. This immunisation schedule also gave rise to specific duodenal antibody secreting cells in seven of eight individuals. Local gastric immunisation resulted in the induction of specific B cells in the gastric mucosa of four of eight volunteers. Gastric antigen application also resulted in B cell responses in the duodenum in all volunteers. Uninfected volunteers receiving the vaccine perorally responded in the duodenum but not in the stomach.
CONCLUSIONS—H pylori infection increases the ability of the gastric mucosa to serve as an expression site for intestinally induced B cell responses. These findings are of importance when designing a therapeutic H pylori vaccine, and based on our results such a vaccine can be delivered along the whole upper gastrointestinal tract.


Keywords: Helicobacter pylori; vaccine; stomach; B cell; lymphocyte traffickin

Homing commitment of lymphocytes activated in the human gastric and intestinal mucosa

BACKGROUND—Gastric infection with the human pathogen Helicobacter pylori results in a large accumulation of IgA and IgM secreting cells in the gastric mucosa. The molecular mechanisms resulting in B cell migration to the gastric mucosa in H pylori infection are however not known.
AIMS—To examine expression of the mucosal homing receptor integrin α4β7 and the homing receptor for secondary lymphoid tissues, L-selectin, on lymphocytes activated by gastric, intestinal, or systemic antigens. Furthermore, to examine gastric expression of the mucosal addressin cellular adhesion molecule 1 (MAdCAM-1), the endothelial counter-receptor to integrin α4β7.
SUBJECTS AND METHODS—H pylori infected individuals were immunised by either gastric (n=8) or intestinal (n=8) delivery of an inactivated cholera vaccine. The resulting circulating vaccine specific B cells were sorted according to α4β7 and L-selectin expression and assayed for production of IgA and IgG using an enzyme linked immunospot assay. In addition, circulating CD4+ T cells from seven H pylori infected individuals were fractionated according to α4β7 and L-selectin expression. The resulting T cell fractions were then assayed for specific proliferation against H pylori or the systemic antigen tetanus toxoid. Finally, gastric expression of MAdCAM-1 was determined by immunohistochemistry in H pylori infected (n=16) and uninfected (n=8) individuals.
RESULTS—Virtually all B cells induced by both gastric and intestinal antigen delivery expressed α4β7 whereas less then half coexpressed L-selectin. Furthermore, H pylori reactive T cells were mainly found in the α4β7+L-selectin+ T cell fraction whereas tetanus specific T cells were largely α4β7−L-selectin+. MAdCAM-1 was present in similar amounts in gastric mucosa from H pylori infected and uninfected individuals.
CONCLUSIONS—B cells and T cells activated by antigens delivered to the gastric mucosa express the mucosal homing receptor integrin α4β7, as do cells activated in the intestine. Together with the observation that gastric endothelial cells express MAdCAM-1, this may partly explain the homing of lymphocytes activated in the stomach or in the small intestine to the gastric mucosa.


Keywords: lymphocyte trafficking; integrin α4β7; L-selectin; stomach; Helicobacter pylor