Rat PYY ELISA Kit

Name: Rat PYY ELISA Kit
SKU: DEIA4773
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

Plasma

Species Reactivity

Rat

Detection Method

cELISA

Intended Use

This ELISA kit is used for quantitative determination of mouse/rat PYY (1-36) and mouse/rat PYY (3-36) in mouse/rat plasma or serum samples.

Contents of Kit

1. Standard
2. Labeled antigen
3. Specific antibody
4. SA-HRP solution
5. Enzyme substrate solution (TMB)
6. Stopping solution
7. Buffer solution
8. Washing solution

Storage

Store the complete kit at 2-8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Detection Range

0.15-12,5 ng/ml

General Description

This ELISA kit is a stable and convenient assay system for peptide YY (PYY). PYY was isolated initially by Tatemoto et al. (1980 ) from the extract of pig duodenum and shown to be a polypeptide consisting of 36 amino acid residues. PYY is homologous to pancreatic polypeptide (PP) and neuropeptide Y (NPY). PYY is localized mainly in endocrine cells in the intestine (ileum, colon, and rectum) showing an inhibitory action on contraction of the gastrointestinal tract and on secretion of pancreatic and gastric juice. PYY is released by taking diet. The PYY level decreases after resection of the intestine possibly are due to the decrease in number of the endocrine cells secreting PYY. The EIA kit is prepared by using synthetic mouse/rat PYY (3-36) as standard antigen and biotinylated mouse/rat PYY (3-36) as labeled antigen. The kit contains specific polyclonal antibody recognized to the amino acid sequence of Mouse/rat PYY. The mouse/rat PYY sequence:
Y-P-A-K-P-E-A-P-G-E-D-A-S-P-E-E-L-S-R-Y-Y-A-S-L-R-H-Y-L-N-L-V-T-R-Q-R-Y-NH2

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Consuming Lower-Protein Nutrition Bars with Added Leucine Elicits Postprandial Changes in Appetite Sensations in Healthy Women

JOURNAL OF NUTRITION

Authors: Bolster, Douglas R.; Rahn, Maike; Kamil, Alison G.; Bristol, Lindsey T.; Goltz, Shellen R.; Leidy, Heather J.; Blaze, Melvin M. T.; Nunez, Michael A.; Guo, Elizabeth; Wang, Jianquan; Harkness, Laura S.

Abstract

Background: Higher-protein meals (>25 g protein/meal) have been associated with enhanced satiety but the role of amino acids is unclear. Leucine has been proposed to stimulate satiety in rodents but has not been assessed in humans. Objective: We assessed the acute effects of lower-protein nutrition bars, enhanced with a leucine peptide (LP), on postprandial appetite sensations in combination with plasma leucine and peptide YY (PYY) in healthy women. Methods: Utilizing a double-blind randomized crossover design, 40 healthy women [28 +/- 7.5 y; body mass index (BMI, in kg/m(2)): 23.5 +/- 2.4] consumed the following isocaloric (180 kcal) pre-loads on 3 separate visits; control bar [9 g protein with 0 g added LP (0-g LP)] or treatment bars [11 g protein with 2 g added LP (2-g LP) or 13 g protein with 3 g added LP (3-g LP)]. Pre- and postprandial hunger, desire to eat, prospective food consumption (PFC), fullness, and plasma leucine were assessed every 30 min for 240 min. Plasma PYY was assessed hourly for 240 min (n = 24). Results: Main effects of time (P < 0.0001) and treatment (P < 0.03) were detected for postprandial hunger, desire to eat, PFC, and fullness. Post hoc analyses revealed that the 2-g and 3-g LP bars elicited greater increases in fullness and greater decreases in PFC compared with 0-g LP (all, P < 0.05) with no differences between the 2-g and 3-g LP bars. The 2-g bar elicited greater decreases in hunger and desire to eat compared with the 0-g LP bar (both, P< 0.01), whereas 3-g LP did not. Appetite incremental areas under the curves (iAUCs) and PYY outcomes were not different between bars. A treatment x time interaction was detected for plasma leucine with increases occurring in a leucine-dose-dependent manner (P < 0.0001). Conclusion: Despite the dose-dependent increases in plasma leucine following the consumption of lower-protein bars enhanced with LP, only the 2-g LP bar elicited consistent postprandial changes in select appetite sensations compared with the 0-g LP bar.

Fructose intervention for 12 weeks does not impair glycemic control or incretin hormone responses during oral glucose or mixed meal tests in obese men

NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES

Authors: Matikainen, N.; Soderlund, S.; Bjornson, E.; Bogl, L. H.; Pietilainen, K. H.; Hakkarainen, A.; Lundbom, N.; Eliasson, B.; Rasanen, S. M.; Rivellese, A.; Patti, L.; Prinster, A.; Riccardi, G.; Despres, J. -P.; Almeras, N.; Holst, J. J.; Deacon, C. F.; Boren, J.; Taskinen, M. -R.

Abstract

Background and aims: Incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are affected early on in the pathogenesis of metabolic syndrome and type 2 diabetes. Epidemiologic studies consistently link high fructose consumption to insulin resistance but whether fructose consumption impairs the incretin response remains unknown. Methods and results: As many as 66 obese (BMI 26-40 kg/m(2)) male subjects consumed fructose-sweetened beverages containing 75 g fructose/day for 12 weeks while continuing their usual lifestyle. Glucose, insulin, GLP-1 and GIP were measured during oral glucose tolerance test (OGTT) and triglycerides (TG), GLP-1, GIP and PYY during a mixed meal test before and after fructose intervention. Fructose intervention did not worsen glucose and insulin responses during OGTT, and GLP-1 and GIP responses during OGTT and fat-rich meal were unchanged. Postprandial TG response increased significantly, p = 0.004, and we observed small but significant increases in weight and liver fat content, but not in visceral or subcutaneous fat depots. However, even the subgroups who gained weight or liver fat during fructose intervention did not worsen their glucose, insulin, GLP-1 or PYY responses. A minor increase in GIP response during OGTT occurred in subjects who gained liver fat (p = 0.049). Conclusion: In obese males with features of metabolic syndrome, 12 weeks fructose intervention 75 g/day did not change glucose, insulin, GLP-1 or GIP responses during OGTT or GLP-1, GIP or PYY responses during a mixed meal. Therefore, fructose intake, even accompanied with mild weight gain, increases in liver fat and worsening of postprandial TG profile, does not impair glucose tolerance or gut incretin response to oral glucose or mixed meal challenge. (C) 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.