Human Agouti-Related Peptide (AgRP) (83-132) amide ELISA Kit

Name: Human Agouti-Related Peptide (AgRP) (83-132) amide ELISA Kit
SKU: DEIA-PP3
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

serum, plasma

Species Reactivity

Human

Intended Use

This kit is designed to measure the concentration of a specific peptide and its related peptides based on the principle of a "competitive" enzyme immunoassay.

Storage

1. Store the kit at 4°C upon receipt.
2. It is highly recommended that solutions be used as soon as possible after rehydration.
3. Store 1x assay buffer at 4°C.
4. Remove any unneeded strips from antibody-coated plate, reseal them in zip-lock foil and keep at 4°C.
5. Keep rehydrated solution of Standard, Biotinylated peptide, Antibody and SA-HRP at 4°C.

Precision

Intra-assay Precision (Precision within an assay): CV%<10%
Inter-assay Precision (Precision between assays): CV%<15%

Detection Range

0-100 ng/ml

Sensitivity

0.09 ng/ml

General Description

Agouti (ASIP) and Agouti-related protein (AgRP) are endogenous antagonists of melanocortin receptors that play critical roles in the regulation of pigmentation and energy balance, respectively, and which arose from a common ancestral gene early in vertebrate evolution. The N-terminal domain of ASIP facilitates antagonism by binding to an accessory receptor. Computational analysis reveals similar patterns of evolutionary constraint in the ASIP and AgRP C-terminal domains, but fundamental differences between the N-terminal domains.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

The association of the fat mass and obesity-associated gene (FTO) rs9939609 polymorphism and the severe obesity in a Brazilian population

DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY

Authors: Proenca da Fonseca, Ana Carolina; Abreu, Gabriella Medeiros; Zembrzuski, Veronica Marques; Campos Junior, Mario; Ivar Carneiro, Joao Regis; Nogueira Neto, Jose Firmino; Cabello, Giselda Maria Kalil; Cabello, Pedro Hernan

Abstract

Background: Obesity occurs due to the interaction between the genetic background and environmental factors, including an increased food intake and a sedentary lifestyle. Nowadays, it is clear that there is a specific circuit, called leptin-melanocortin pathway, which stimulates and suppresses food intake and energy expenditure. Therefore, the aim of this study was to evaluate the influence of genetic variants related to appetite regulation and energy expenditure on severe obesity susceptibility and metabolic phenotypes in a Brazilian cohort. Material and methods: A total of 490 participants were selected (298 severely obese subjects and 192 normal-weight individuals). Genomic DNA was extracted and polymorphisms in protein related to agouti (AGRP; rs5030980), ghrelin (GHRL; rs696217), neuropeptide Y (NPY, rs535870237), melanocortin 4 receptor (MC4R; rs17782313), brain-derived neurotrophic factor (BDNF; rs4074134) and fat mass and obesity-associated (FTO; rs9939609) genes were genotyped using TaqMan (R) probes. Demographic, anthropometric, biochemical and blood pressure parameters were obtained from the participants. Results: Our results showed that FTO rs9939609 was associated with severe obesity susceptibility. This polymorphism was also related to body weight, body mass index (BMI), waist to weight ratio (WWR) and inverted BMI. Individuals carrying the mutant allele (A) showed higher levels of BMI as well as lower values of WWR and inverted BMI. Conclusion: This study showed that FTO rs9939609 polymorphism plays a significant role in predisposing severe obesity in a Brazilian population.

Hypoglycemia-activated Hypothalamic Microglia Impairs Glucose Counterregulatory Responses

SCIENTIFIC REPORTS

Authors: Winkler, Zsuzsanna; Kuti, Daniel; Polyak, Agnes; Juhasz, Balazs; Gulyas, Krisztina; Lenart, Nikolett; Denes, Adam; Ferenczi, Szilamer; Kovacs, Krisztina J.

Abstract

Glucose is a major fuel for the central nervous system and hypoglycemia is a significant homeostatic stressor, which elicits counterregulatory reactions. Hypothalamic metabolic-and stress-related neurons initiate these actions, however recruitment of glia in control such adaptive circuit remain unknown. Groups of fed-and fasted-, vehicle-injected, and fasted + insulin-injected male mice were compared in this study. Bolus insulin administration to fasted mice resulted in hypoglycemia, which increased hypothalamo-pituitary-adrenal (HPA) axis-and sympathetic activity, increased transcription of neuropeptide Y (Npy) and agouti-related peptide (Agrp) in the hypothalamic arcuate nucleus and activated IBA1+ microglia in the hypothalamus. Activated microglia were found in close apposition to hypoglycemia-responsive NPY neurons. Inhibition of microglia by minocycline increased counterregulatory sympathetic response to hypoglycemia. Fractalkine-CX3CR1 signaling plays a role in control of microglia during hypoglycemia, because density and solidity of IBA1-ir profiles was attenuated in fasted, insulin-treated, CX3CR1 KO mice, which was parallel with exaggerated neuropeptide responses and higher blood glucose levels following insulin administration. Hypoglycemia increased Il-1b expression in the arcuate nucleus, while IL-1a/b knockout mice display improved glycemic control to insulin administration. In conclusion, activated microglia in the arcuate nucleus interferes with central counterregulatory responses to hypoglycemia. These results underscore involvement of microglia in hypothalamic regulation of glucose homeostasis.