Peptide YY ELISA Kit

BackgroundFeeding triggers inter-related gastrointestinal (GI) motor, peptide and appetite responses. These are rarely studied together due to methodological limitations. Recent MRI advances allow pan-intestinal, non-invasive assessment of motility in the undisturbed gut. This study aimed to develop a methodology to assess pan-intestinal motility and transit in a single session using MRI and compare imaging findings to GI peptide responses to a test meal and symptoms in a healthy volunteer cohort. MethodsFifteen healthy volunteers (29.32.7years and BMI 20.11.2kgm(-2)) underwent baseline and postprandial MRI scans, symptom questionnaires, and blood sampling (for subsequent GI peptide analysis, Glucagon-like peptide-1 [GLP-1], Polypeptide YY [PYY], Cholecystokinin [CCK]) at intervals for 270minutes following a 400g soup meal (204kcal, Heinz, UK). Gastric volume, gall bladder volume, small bowel water content, small bowel motility, and whole gut transit were measured from the MRI scans. Key Results(mean +/- SEM) Small bowel motility index increased from fasting 39 +/- 3 arbitrary units (a.u.) to a maximum of 87 +/- 7a.u. immediately after feeding. PYY increased from fasting 98 +/- 10pgmL(-1) to 149 +/- 14pgmL(-1) at 30minutes and GLP-1 from fasting 15 +/- 3gmL(-1) to 22 +/- 4gmL(-1). CCK increased from fasting 0.40 +/- 0.06pmolmL(-1) to 0.94 +/- 0.1pmolmL(-1). Gastric volumes declined with a T-1/2 of 46 +/- 5minute and the gallbladder contracted from a fasting volume of 19 +/- 2mL(-1) to 12 +/- 2mL(-1). Small bowel water content increased from 39 +/- 2mL(-1) to 51 +/- 2mL(-1) postprandial. Fullness VAS score increased from 9 +/- 5mm to 41 +/- 6mm at 30minutes postprandial. Conclusions and InferencesThe test meal challenge was effective in inducing a change in MRI motility end-points which will improve understanding of the pathophysiological postprandial GI response.

We hypothesized that peptide YY (PYY) is involved in the metabolic regulation of food intake in fish. Therefore, we assessed in rainbow trout (Oncorhynchus mykiss) the effects of intracerebroventricular treatment with 10 ng/g PYY1-36 on food intake, expression of neuropeptides involved in food intake control, and the activity of fatty acid-sensing systems. The administration of PYY1-36 caused a significant reduction in food intake up to 24 h post-treatment. This anorectic action was associated with changes 2 h after treatment in mRNA abundance of neuropeptides involved in metabolic regulation of food intake in hypothalamus (decreased NPY and raised CART values) and hindbrain (increased POMCa1 values). We also observed that PYY1-36 treatment induced changes in mRNA abundance of parameters related to fatty acid sensing and metabolism in hypothalamus (decreased values of ACLY, PPAR gamma, and SREBP1c) and hindbrain (increased values of LPL, FAT/CD36, PPAR alpha, PPAR gamma, and SREBP1c and decreased values of UCP2a). PYY1-36 treatment also increased mRNA abundance of mTOR. In general, it seems that mRNAs encoding some components of the machinery required for fatty acid sensing and metabolism are activated by PYY1-36. The response observed was higher in the hindbrain than in the hypothalamus, supporting the greater importance of this brain area in mediating the modulatory effects of gastrointestinal hormones on feeding regulation.