PYYT-66HK Sigma-AldrichHuman PYY (Total) RIA

The site of intestinal fat delivery affects satiety and may affect food intake in humans. Animal data suggest that the length of the small intestine exposed to fat is also relevant. The aim of the present study was to investigate whether increasing the areas of intestinal fat exposure and the way it is exposed would affect satiety parameters and food intake. In the present single-blind, randomised, cross-over study, fifteen volunteers, each intubated with a naso-ileal tube, received four treatments on consecutive days. The oral control (control treatment) was a liquid meal (LM) containing 6 g fat ingested at t = 0 min, with saline infusion at t = 30-120 min. Experimental treatments were a fat-free LM at t = 0 min, with either 6 g oil delivered sequentially (2 g duodenal, t = 30-60 min; 2 g jejunal, t = 60-90 min; 2 g ileal, t = 90-120 min), simultaneously (2 g each to all sites, t = 30-120 min) or ileal only (6 g ileal, t = 30-120 min). Satiety parameters (hunger and fullness) and cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY) secretion were measured until t = 180 min, when ad libitum food intake was assessed. Only the ileum treatment reduced food intake significantly over the control treatment. The ileum and simultaneous treatments significantly reduced hunger compared with the control treatment. Compared with control, no differences were observed for PYY, CCK and GLP-1 with regard to 180 min integrated secretion. Ileal fat infusion had the most pronounced effect on food intake and satiety. Increasing the areas of intestinal fat exposure only affected hunger when fat was delivered simultaneously, not sequentially, to the exposed areas. These results demonstrate that ileal brake activation offers an interesting target for the regulation of ingestive behaviour.

A cross-sectional study was carried out in order to compare intestinal microbiological and immunological biomarkers with blood glucose and lipids, satiety-related hormones and inflammatory biomarkers characterising differences between obese and normal weight subjects. Faecal and blood samples were obtained from twenty obese subjects with an average BMI of 32.9 kg/m2 and twenty normal weight subjects with an average BMI of 23.3 kg/m2. Blood insulin, TAG and leptin were significantly elevated, whereas concentrations of HDL and ghrelin were significantly decreased in the obese subjects. Inflammatory status in the obese subjects was characterised by a trend for elevated blood C-reactive protein (CRP; P = 0.06) and IL-6 (P = 0.02). The faecal microbial composition differed between the groups; less sulphate-reducing bacteria (P = 0.05) and a trend for less Bacteroides (P = 0.07) were measured for overweight subjects. Furthermore, an inverse correlation was demonstrated between faecal Bacteroides levels and waist circumference (P = 0.05). The faecal microbial metabolites differed between the groups; increased concentrations of branched-chain fatty acids, phenolics, valeric acid, di- and hydroxy acids were described in the obese subjects. No differences between the measured intestinal inflammatory biomarkers were detected. However, systemic inflammation (CRP and IL-6) was correlated with the faecal concentrations of phenolics and lactic acid (P < 0.05 and 0.05, and P < 0.01 and 0.05, respectively). In summary, weight-related differences were observed both in the intestinal microbial composition and its activity. The role of intestinal signals, such as phenolics and lactic acid in the development of weight-related problems, needs to be studied further.