Peptídeo-C Canino RIE

Canine C-Peptide RIA

Peptídeo-C é um bioproduto da produção normal de insulina pelas células beta do pâncreas e se correlaciona diretamente com concentrações endógenas de insulina.

Aplicações:
Incubação de equilíbrio overnight a 4°C. Volume de amostra < 100 µL soro, plasma, ou meio de cultura de tecido.

Reatividade:  Canino

Precisão, %: 

• Inter-ensaio: 5.61-6.91
• Intra-ensaio: 3.06-3.33

Áreas terapêuticas: 

• Diabetes
• Obesidade
• Desordem Metabólica

Sensibilidade: 0.15 ng/mL

Exatidão:  97-111%

Intervalo da curva:  0.156–20 ng/mL

Antígeno: aa1-aa31-OVA via glutaraldehyde

UniProt Number: P01321

Linearidade de Diluição: 95-101%

Desempenho: 

• ED₈₀ = 0.56 ± 0.15 ng/mL
• ED₅₀ = 2.03 ± 0.54 ng/mL
• ED₂₀ = 7.21 ± 2.76 ng/mL

Proteína: C-Peptide

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

Documento

Protocolo

Referência

Elevated glucagon-like peptide-1-(7-36)-amide, but not glucose, associated with hyperinsulinemic compensation for fat feeding.

Abstract

We previously developed a canine model of central obesity and insulin resistance by supplementing the normal chow diet with 2 g cooked bacon grease/kg body weight. Dogs fed this fatty diet maintained glucose tolerance with compensatory hyperinsulinemia. The signal(s) responsible for this up-regulation of plasma insulin is unknown. We hypothesized that meal-derived factors such as glucose, fatty acids, or incretin hormones may signal beta-cell compensation in the fat-fed dog. We fed the same fat-supplemented diet for 12 wk to six dogs and compared metabolic responses with seven control dogs fed a normal diet. Fasting and stimulated fatty acid and glucose-dependent insulinotropic peptide concentrations were not increased by fat feeding, whereas glucose was paradoxically decreased, ruling out those three factors as signals for compensatory hyperinsulinemia. Fasting plasma glucagon-like peptide-1 (GLP-1) concentration was 2.5-fold higher in the fat-fed animals, compared with controls, and 3.4-fold higher after a mixed meal. Additionally, expression of the GLP-1 receptor in whole pancreas was increased 2.3-fold in the fat-fed dogs. The increase in both circulating GLP-1 and its target receptor may have increased beta-cell responsiveness to lower glucose. Glucose is not the primary cause of hyperinsulinemia in the fat-fed dog. Corequisite meal-related signals may be permissive for development of hyperinsulinemia.