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Mouse insulin elisa

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The Mouse Insulin ELISA is a laboratory equipment used to measure the concentration of insulin in mouse samples. It employs the Enzyme-Linked Immunosorbent Assay (ELISA) technique to quantify the amount of insulin present in the sample.

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Lab products found in correlation

Mouse leptin elisa, by Crystal Chem (3 mentions) Contour glucometer, by Bayer (1 mentions) Enzymatic colorimetric assay kits, by Wiener Lab (1 mentions) Mouse adiponectin elisa kit, by Crystal Chem (1 mentions) Mouse creatinine assay, by Crystal Chem (1 mentions) Mouse ccl 20 mip 3 alpha quantikine elisa kit, by R&D Systems (1 mentions) Mouse albumin elisa quantification set, by Fortis Life Sciences (1 mentions)

Spelling variants of this product

Insulin (75 citations) Ultra Sensitive Mouse Insulin ELISA (51 citations) Insulin ELISA (15 citations) Mouse ultrasensitive insulin ELISA kit (12 citations) Mouse Ultrasensitive Insulin ELISA (10 citations) Rat/mouse insulin ELISA kit (6 citations) Ultra Mouse Insulin ELISA Kit (4 citations) ELISAs (3 citations) Mouse/rat Insulin ELISA (3 citations) Mouse insulin enzyme-linked immunosorbent assay (ELISA) kit (2 citations)

7 protocols using mouse insulin elisa

1

Measuring Plasma Glucose and Gut Hormones

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Blood glucose concentrations were determined using a glucometer (Elite, Bayer Inc.) from fresh tail-vein blood. In order to determine active levels of GLP-1, mice were orally administered a single dose of Intralipid (20%) containing D-glucose (30%) via oral gavage and blood collected 20 min post-dose (Althage et al., 2008 (link); Lu et al., 2007 (link)) into pre-chilled tubes containing EDTA, aprotinin and DPP-4 inhibitor. Plasma insulin was measured with a mouse insulin ELISA (Crystal Chem Inc., Downers Grove, IL) and active GLP-1 determined with the GLP-1 (Active 7–36) ELISA (ALPCO, Salem, NH). Plasma GIP and leptin were analyzed in 100 μl of plasma (final bleed) using a MILLIPLEX Mouse Gut Hormone Magnetic Bead Panel (Millipore, Billerica, MA). HOMA-IR, a measure of liver insulin sensitivity, was quantified by: fasting insulin (μU/mL) x fasting glucose (mg/dL)/405 (Haffner et al., 1997 (link)).
González-Mariscal I., Krzysik-Walker S.M., Kim W., Rouse M, & Egan J.M. (2015). Blockade of Cannabinoid 1 Receptor Improves GLP-1R Mediated Insulin Secretion in Mice. Molecular and cellular endocrinology, 423, 1-10.
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2

Glucose and Insulin Profiling in Mice

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Fed and fasted blood samples were collected from mice via tail vein or trunk bleeds using a capillary blood collection system (Sarstedt, Nümbrecht) and blood glucose was measured using a Contour glucometer (Bayer Corp). Fasted blood samples were collected after a 16 h overnight fast. Plasma insulin levels were analysed using a mouse insulin ELISA (Crystalchem Inc.).
Irvine E.E., Katsouri L., Plattner F., Al-Qassab H., Al-Nackkash R., Bates G.P, & Withers D.J. (2019). Genetic deletion of S6k1 does not rescue the phenotypic deficits observed in the R6/2 mouse model of Huntington’s disease. Scientific Reports, 9, 16133.
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3

Biochemical Profiling for Metabolic Health

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Serum cholesterol and triglycerides were measured with enzymatic colorimetric assay kits (Wiener Lab, Rosario, Argentina). Serum insulin and adiponectin levels were assessed by ELISA using the ultrasensitive mouse insulin ELISA (catalog 90080) and mouse adiponectin ELISA kit (catalog 80569) from Crystal Chem (Downers Grove, IL, USA).
The homeostasis model assessment of basal insulin resistance (HOMA-IR) was used to calculate an index from the product of the fasting concentrations of serum glucose (mmol/l) and serum insulin (μU/ml) divided by 22.5 (Matthews et al., 1985 (link)). Lower HOMA-IR values indicated greater insulin sensitivity, whereas higher HOMA-IR values indicated lower insulin sensitivity (insulin resistance).
Quiroga D.T., Miquet J.G., Gonzalez L., Sotelo A.I., Muñoz M.C., Geraldes P.M., Giani J.F, & Dominici F.P. (2019). Mice lacking angiotensin type 2 receptor exhibit a sex-specific attenuation of insulin sensitivity. Molecular and cellular endocrinology, 498, 110587.
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4

Metabolic Biomarkers in Whole Blood

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Blood glucose levels were determined from whole venous blood using an automatic glucose monitor (Bayer Contour, Bayer, Germany). Leptin and insulin levels in serum were measured by ELISA using mouse standards according to manufacturer’s guidelines (Mouse Leptin ELISA; Crystal Chem, IL, USA/Mouse Insulin ELISA; Crystal Chem, IL, USA). Serum non-esterified free fatty acids (NEFA) were quantified with according to the manufacturer’s instructions (WAKO Chemicals GmbH, Germany). Liver and serum triglyceride concentrations were determined in 6 hour fasted animals. Liver triglycerides were extracted as previously described46 (link). Liver and serum triglyceride content was quantified according to the manufacturer’s instructions (Sigma, USA).
Mauer J., Chaurasia B., Goldau J., Vogt M.C., Ruud J., Nguyen K.D., Theurich S., Hausen A.C., Schmitz J., Brönneke H.S., Estevez E., Allen T.L., Mesaros A., Partridge L., Febbraio M.A., Chawla A., Wunderlich F.T, & Brüning J.C. (2014). Interleukin-6 signaling promotes alternative macrophage activation to limit obesity-associated insulin resistance and endotoxemia. Nature immunology, 15(5), 423-430.
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5

Metabolic Biomarkers in Whole Blood

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Blood glucose levels were determined from whole venous blood using an automatic glucose monitor (Bayer Contour, Bayer, Germany). Leptin and insulin levels in serum were measured by ELISA using mouse standards according to manufacturer’s guidelines (Mouse Leptin ELISA; Crystal Chem, IL, USA/Mouse Insulin ELISA; Crystal Chem, IL, USA). Serum non-esterified free fatty acids (NEFA) were quantified with according to the manufacturer’s instructions (WAKO Chemicals GmbH, Germany). Liver and serum triglyceride concentrations were determined in 6 hour fasted animals. Liver triglycerides were extracted as previously described46 (link). Liver and serum triglyceride content was quantified according to the manufacturer’s instructions (Sigma, USA).
Mauer J., Chaurasia B., Goldau J., Vogt M.C., Ruud J., Nguyen K.D., Theurich S., Hausen A.C., Schmitz J., Brönneke H.S., Estevez E., Allen T.L., Mesaros A., Partridge L., Febbraio M.A., Chawla A., Wunderlich F.T, & Brüning J.C. (2014). Interleukin-6 signaling promotes alternative macrophage activation to limit obesity-associated insulin resistance and endotoxemia. Nature immunology, 15(5), 423-430.
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6

Serum Biomarker Measurement Protocol

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The blood glucose was measured by a glucometer (CareSens, Seoul, Korea). To avoid diurnal variation in blood glucose, all measurements were conducted in the same time slot every week. The blood samples were left to stand for 30 min at room temperature, followed by centrifugation at 2000 rpm for 10 min at 4 °C. Serums were collected and stored at −80 °C until analysis. Serum creatinine concentration was determined by Mouse Creatinine Assay (Crystal Chem, Elk Grove Village, IL, USA) as per the manufacturer’s instructions. Serum insulin and TGF-β1 concentrations were determined by Mouse Insulin ELISA and Mouse TGF-β1 ELISA (Crystal Chem), respectively.
Mok H., Al-Jumaily A, & Lu J. (2022). Plasmacytoma Variant Translocation 1 (PVT1) Gene as a Potential Novel Target for the Treatment of Diabetic Nephropathy. Biomedicines, 10(11), 2711.
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7

Measuring Inflammatory and Metabolic Markers

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The concentrations of leptin and insulin in serum, CCL-20 in the supernatent of cultured BMDM and albumin in the faeces were measured by enzyme-linked immunosorbent assays, with mouse standards, according to manufacturer’s guidelines.: Mouse Leptin ELISA (90030, Crystal Chem), Mouse Insulin ELISA (90080, Crystal Chem), Mouse CCL-20/MIP-3 alpha Quantikine ELISA Kit (MCC200, R&D Systems) and Mouse Albumin ELISA Quantification set (E90-134,Bethyl).
Wunderlich C.M., Ackermann P.J., Ostermann A.L., Adams-Quack P., Vogt M.C., Tran M.L., Nikolajev A., Waisman A., Garbers C., Theurich S., Mauer J., Hövelmeyer N, & Wunderlich F.T. (2018). Obesity exacerbates colitis-associated cancer via IL-6-regulated macrophage polarisation and CCL-20/CCR-6-mediated lymphocyte recruitment. Nature Communications, 9, 1646.
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