Resistina de Camundongo - ELISA

Descrição: Mouse Resistin ELISA

Informação: Resistina  de camundongo (Mouse Resistin) é um novo membro da grande família das Adipoquinas e é também conhecida como ADSF (adipocyte specific secretory factor) e FIZZ3 (encontrado em zonas inflamatórias).  A resistina de camundongo é uma proteína de 94 aminoácidos produzida nos adipócitos. Esta proteína é um elo perdido de ligação entre obesidade, resitência a insulina e diabetes tipo 2. Os níveis de Resistina de camundongo aumentam com a obesidade em vários modelos de camundongo. Sua administração exógena enfraquece a tolerância a glicose e a ação da insulina. Dosagem de resistina de camundongo sob diferentes situações patofisiológicas, nutrcionais e genéticas resultam no melhor entendimento da etiologia da diabetes tipo 2 e obesidade.

Este kit é destinado a quantificação de resistina de camundongo em soro, plasma ou tecido.

Aplicações: 

Temperatura ambiente, 3.5 horas com 20 µL de amostra

Reatividade: Humano

Precisão, %:

• Inter-ensaio: 2.9–5.4  
• Intra-ensaio: 5.0–10.3

Sensibilidade: 0.78 ng/mL

Áreas terapêuticas:

• Diabetes
• Obesidade
• Desordem Metabólica

Exatidão: 90–102%

Intervalo da curva: 0.78–50 ng/mL

UniProt Number:

• Q99P87
• Q9HD89  

Linearidade de diluição: 92–113% 

Proteína: Resistin

Somente para pesquisa, não é destinado ao uso terapêutico ou diagnóstico.

DOCUMENTOS

 Protocolo

Referências

Defective peripheral nerve development is linked to abnormal architecture and metabolic activity of adipose tissue in Nscl-2 mutant mice.

Author	Karen Ruschke, Henning Ebelt, Nora Klöting, Thomas Boettger, Kay Raum, Matthias Blüher, Thomas Braun
Citation Information	PloS one, 4:e5516 (2009)
Keywords	Adipose Tissue, White, Animals, Basic Helix-Loop-Helix Transcription Factors, Female, Glucose, Insulin, Leptin, Male, Mice, Mice, Inbred Strains, Mutation, Peripheral Nerves
Related Products	EZMR-96K, EZRMI-13K, ML-82K
Pub Med ID	19436734

Abstract

[Full Text Article]

BACKGROUND: In mammals the interplay between the peripheral nervous system (PNS) and adipose tissue is widely unexplored. We have employed mice, which develop an adult onset of obesity due to the lack the neuronal specific transcription factor Nscl-2 to investigate the interplay between the nervous system and white adipose tissue (WAT). METHODOLOGY: Changes in the architecture and innervation of WAT were compared between wildtype, Nscl2-/-, ob/ob and Nscl2-/-//ob/ob mice using morphological methods, immunohistochemistry and flow cytometry. Metabolic alterations in mutant mice and in isolated cells were investigated under basal and stimulated conditions. PRINCIPAL FINDINGS: We found that Nscl-2 mutant mice show a massive reduction of innervation of white epididymal and paired subcutaneous inguinal fat tissue including sensory and autonomic nerves as demonstrated by peripherin and neurofilament staining. Reduction of innervation went along with defects in the formation of the microvasculature, accumulation of cells of the macrophage/preadipocyte lineage, a bimodal distribution of the size of fat cells, and metabolic defects of isolated adipocytes. Despite a relative insulin resistance of white adipose tissue and isolated Nscl-2 mutant adipocytes the serum level of insulin in Nscl-2 mutant mice was only slightly increased. CONCLUSIONS: We conclude that the reduction of the innervation and vascularization of WAT in Nscl-2 mutant mice leads to the increase of preadipocyte/macrophage-like cells, a bimodal distribution of the size of adipocytes in WAT and an altered metabolic activity of adipocytes