Insulin ELISA Kit

Overview

Product name

Human Insulin ELISA Kit

Detection method: colorimetric

Human Insulin ELISA Kit for serum, plasma, cell culture supernatants and  urine | Sigma-Aldrich

Example type

Cell culture supernatant, Serum, Plasma

Essay type: sandwich (quantitative)

Sensitivity: < 4 µIU/mL

Distance: 4.69 µlU/ml – 300 µlU/ml

Recovery: 89%

Test duration: Standard multi-step assay

Species reactivity

  • Reacts with: Human
  • Intended to work with: Mouse, Rat, Cow, Pig

Product description

Abcam’s Human Insulin ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human insulin and proinsulin in serum, plasma and cell culture supernatants. This assay employs an antibody specific for human insulin coated on a 96-well plate. Standards and samples are pipetted into the wells and insulin present in a sample are bound to the wells by the immobilized antibody.

The wells are washed and a biotinylated anti-human insulin antibody is added. After washing away the unbound biotinylated antibody, the HRP-conjugated streptavidin is pipetted into the wells. The wells are again washed, a TMB substrate solution is added to the wells and the colour develops in proportion to the amount of insulin bound. The stop solution changes colour from blue to yellow and the intensity of the colour is measured at 450 nm.

Grades: Optimization with urine samples may be required.

Platform: microplate

Properties

Storage instructions

Store at -20°C. Check the protocols.

Function

Insulin lowers the concentration of glucose in the blood. Increases cell permeability to monosaccharides, amino acids and fatty acids. Accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in the liver.

Involvement in the disease

Defects in the INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:176730]. Defects in the INS are a cause of insulin-dependent diabetes mellitus type 2 (IDDM2) [MIM:125852]. IDDM2 is a multifactorial disorder of glucose homeostasis characterized by susceptibility to ketoacidosis in the absence of insulin therapy. The clinical features are polydipsia, polyphagia, and polyuria resulting from hyperglycemia-induced osmotic diuresis and secondary thirst. These disorders result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.

Defects in the INS are a cause of permanent neonatal diabetes mellitus (PNDM) [MIM:606176]. PNDM is a rare form of diabetes other than childhood-onset autoimmune type 1 diabetes mellitus. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first few months of life. Permanent neonatal diabetes requires lifelong therapy.

Defects in the INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:613370]. MODY10 is a form of diabetes characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before the age of 25 years), a primary defect in insulin secretion, and frequent insulin independence. insulin at the beginning of the disease.

Sequence similarities

It belongs to the family of insulins.

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