God pap

Manufactured by Roche

Sourced in Spain

The GOD-PAP is a laboratory equipment product designed for the quantitative determination of glucose. It utilizes the glucose oxidase-peroxidase (GOD-PAP) method to measure glucose levels in biological samples.

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Lab products found in correlation

Lpl gop trinder, by Roche (2 mentions) Acs acod, by Fujifilm (2 mentions) Hr series nefa hr, by Fujifilm (1 mentions) Milliplex madpk 71k adipokine kit, by Merck Group (1 mentions) Microplate imaging system, by Bio-Rad (1 mentions) Protein assay kit, by Bio-Rad (1 mentions) Colorimetric assay, by Fujifilm (1 mentions) Double antibody radioimmunoassay, by Linco Research (1 mentions) Chod pod, by Spinreact (1 mentions) Contraa 700, by Analytik Jena (1 mentions) Elecsys 1010 2010, by Roche (1 mentions) Streptozotocin (stz), by Merck Group (1 mentions)

Close spelling variants of this product

GLU Glucose GOD-PAP Glucose GOD-PAP

11 protocols using god pap

Comprehensive Metabolic Profiling Protocol

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Glucose was measured with the glucose-oxidase GOD-PAP method (Roche Diagnostics, Mannheim, Germany). Plasma levels of triglycerides, uric acid, and transaminases (aspartate aminotransferase-GOT and alanine aminotransferase-GPT) were assayed by commercial (enzymatic-colorimetric) kits (Wiener Lab., Rosario, Santa Fe, Argentina). Circulating immunoreactive insulin was determined by a previously described specific radioimmunoassay [38 (link)].
Glycemia and insulin values were used to estimate peripheral IR by homeostasis model assessment of insulin resistance (HOMA-IR) (insulin × glycemia/22.5) [39 (link)] and β-cell function by HOMA-β [(20 × insulin/glycemia) − 3.5]. Liver insulin sensitivity index (LISI) was calculated by the following formula: k/(fasting plasma insulin) × fasting glycemia, where k = 22.5 × 18 (insulin/glycemia) [40 (link)]. Insulin and glycemia were expressed as μUI/mL and mM, respectively.

Castro M.C., Villagarcía H.G., Di Sarli Gutiérrez L., Arbeláez L.G., Schinella G., Massa M.L, & Francini F. (2024). Akt Signaling and Nitric Oxide Synthase as Possible Mediators of the Protective Effect of N-acetyl-L-cysteine in Prediabetes Induced by Sucrose. International Journal of Molecular Sciences, 25(2), 1215.

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Assessing Metabolic Biomarkers and Insulin Resistance

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Glucose, triglycerides and non-esterified free fatty acids were assayed by enzymatic colorimetric tests (GOD-PAP, LPL/GOP-Trinder, Roche Diagnostics, Basil, Switzerland and HR Series NEFA-HR, Wako Diagnostics, Neuss, Germany). Plasma levels of insulin were measured using a Milliplex MADPK-71K adipokine kit (Merck-Millipore, Burlington, MA, USA) according to the manufacturer’s instructions. For estimation of insulin resistance, HOMA index was calculated as HOMA-IR = (FPG × FPI)/2430, where FPI was in microunits per milliliter and FPG in milligram per deciliter, as previously described [35 (link)].

Alcala M., Bolado V.E., Sánchez-Vera I., Clapés S., Dasí F., Sáez G., Carrera E., Alvarez-Gallego F., Loeken M.R, & Viana M. (2021). Prevention of Teratogenesis in Pregnancies of Obese Rats by Vitamin E Supplementation. Antioxidants, 10(8), 1173.

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Metabolic Biomarker Measurement Protocol

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Glucose and triglycerides were determined by enzymatic colorimetric test (GOD-PAP and LPL/GOP-Trinder, Roche Diagnostics, Barcelona, Spain). Plasma levels of insulin were measured using a Milliplex MADPK-71K adipokine kit according to manufacturer´s description (Millipore). For estimation of insulin resistance HOMA index was calculated as previously described [26 (link)]. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzymatic activities were measured using an commercial kit (GPT/ALT and GOT/AST, Sinreact, Spain).

Alcala M., Calderon-Dominguez M., Serra D., Herrero L., Ramos M.P, & Viana M. (2017). Short-term vitamin E treatment impairs reactive oxygen species signaling required for adipose tissue expansion, resulting in fatty liver and insulin resistance in obese mice. PLoS ONE, 12(10), e0186579.

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Metabolic Biomarker Analysis Protocol

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Plasma glucose concentration was measured colorimetrically (glucose oxidase-phenol and 4
aminophenazone (GOD-PAP) method; Roche Diagnostics) and analysed using a micro plate
imaging system (Bio-Rad Laboratories, Inc.). Insulin concentration was measured using
ELISA (DRG) according to the manufacturer’s protocol. Homoeostasis model assessment of
insulin resistance as calculated from fasting plasma glucose and insulin concentrations
(glucose (mmol/l)×insulin (pmol/l)/22·5) as an indirect measure of insulin sensitivity.
Total cholesterol, HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol and TAG
concentrations were determined colorimetrically after enzymatic conversion using a Roche
Hitachi 717 analyzer (Reinier de Graaf Laboratory).

Baars A., Oosting A., Engels E., Kegler D., Kodde A., Schipper L., Verkade H.J, & van der Beek E.M. (2016). Milk fat globule membrane coating of large lipid droplets in the diet of young mice prevents body fat accumulation in adulthood. The British Journal of Nutrition, 115(11), 1930-1937.

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Plasma Metabolic and Hormonal Analysis

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Glycemia was measured by the glucose-oxidase GOD-PAP method (Roche Diagnostics, Mannheim, Germany) and plasma concentrations of triglycerides, uric acid, and transaminases aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) were determined by commercial (enzymatic-colorimetric) assays (Wiener Lab, Argentina). Peripheral immunoreactive insulin [13 (link)], leptin, and corticosterone [16 (link)] levels were determined by previously described specific radioimmunoassays. Lipid peroxidation was estimated by measuring TBARS (thiobarbituric acid-reactive substance) [20 (link)]. The amount of TBARS formed was calculated by extinction coefficient of the MDA (malondialdehyde)-TBA complex of 1.56 × 105 (mol/L)⁻¹·cm⁻¹ and expressed as pmol of MDA/mg of plasma protein per mL of plasma, measured with the Bio-Rad Protein Assay kit.
Fasting glycemia and insulin values were used to estimate peripheral insulin resistance by homeostasis model assessment-insulin resistance (HOMA-IR) [insulin (μUI/mL) × glycemia (mM)/22.5]. Liver insulin sensitivity index (LISI) was calculated with the following formula: k/(fasting plasma insulin) × fasting glycemia, where k = 22.5 × 18 [21 (link)].

Villagarcía H.G., Sabugo V., Castro M.C., Schinella G., Castrogiovanni D., Spinedi E., Massa M.L, & Francini F. (2016). Chronic Glucocorticoid-Rich Milieu and Liver Dysfunction. International Journal of Endocrinology, 2016, 7838290.

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Metabolic Responses to Mixed Meal

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After an overnight fast, participants were given a 3-h mixed meal challenge (500 kcal, 60% CHO, 20% fat, and 20% protein). Blood samples were collected at 0, 30, 60, 90, 120, and 180 min for plasma glucose, insulin, proinsulin, triglycerides, and glucagon measurements. Glucose was assessed using a glucose-oxidase method (GOD/PAP, Roche Diagnostics, Germany). Insulin was assessed by a chemiluminescent method (Roche Diagnostics, Germany). Proinsulin and glucagon were assessed by a double-antibody radioimmunoassay (Linco Research, USA). Free fatty acid fasting levels were assessed by a colorimetric assay (Wako, USA). Subjects were instructed to refrain from physical exercise, alcohol, and caffeine intake 24 h prior to the test.

Benatti F.B., Miyake C.N., Dantas W.S., Zambelli V.O., Shinjo S.K., Pereira R.M., Silva M.E., Sá-Pinto A.L., Borba E., Bonfá E, & Gualano B. (2018). Exercise Increases Insulin Sensitivity and Skeletal Muscle AMPK Expression in Systemic Lupus Erythematosus: A Randomized Controlled Trial. Frontiers in Immunology, 9, 906.

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Biochemical Markers of Metabolism

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Glucose ((GOD-PAP); Roche Diagnostics, Barcelona, Spain), triacylglycerides ((LPL- GPO); Roche Diagnostics), cholesterol ((CHOD-POD); Spinreact, Girona, Spain), glycerol (GPO-Trinder, Sigma Diagnostic, Madrid, Spain) and NEFA ((ACS-ACOD); Wako Chemicals, Neuss, Germany) levels were determined by enzymatic colorimetric tests. Plasma insulin measurement (Mercodia, Uppsala, Sweden) was determined using immunoassay kits. The HOMA-IR insulin resistance index and QUICKI insulin sensitivity index were calculated as previously described [33 (link)].

Zuccaro A., Zapatería B., Sánchez-Alonso M.G., Haro M., Limones M., Terrados G., Izquierdo A., Corrales P., Medina-Gómez G., Herradón G., Sevillano J, & Ramos-Álvarez M.D. (2021). Pleiotrophin Deficiency Induces Browning of Periovarian Adipose Tissue and Protects against High-Fat Diet-Induced Hepatic Steatosis. International Journal of Molecular Sciences, 22(17), 9261.

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Hormonal Profile Assessment Protocol

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Venous blood samples were obtained from the antecubital area by phlebotomy between the hours of 08:00 and 09:00 following 10-12 h of fasting. After these samples were allowed to clot, they were centrifuged for 10 minutes at 3000 g. The sera were separated and stored at -70°C until the analysis.
Plasma glucose levels were measured by enzymatic colorimetric assay (GOD-PAP, Roche Diagnostics, Mannheim). Plasma zinc and copper levels were measured by atomic absorption spectrophotometry (ContrAA700, Analytik Jena AG, Germany) with an intra-assay CV of 2.4% and an inter-assay CV of 3.1%. Electrochemoluminescence immunoassay was used to measure serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol, prolactin and 17-hydroxy-progesterone (Roche Elecsys 1010/2010, Roche Diagnostics, Mannheim, Germany). The serum concentrations of dehidroepiandrosterone sulphate (DHEAS), thyroid stimulating hormone (TSH), total testosterone, free testosterone and insulin were measured by radioimmunoassay (DSL Diagnostic Systems Laboratories, USA). The intra-assay CVs were 5.3%, 3.8%, 7.8%, 6.2%, 5.0%, 9.6%, 10.0%, 9.6%, 9.7% and 8.2% whereas the inter-assay CVs were 1.8%, 1.5%, 10.0%, 5.7%, 4.1%, 9.3%, 7.8%, 6.6%, 6.2% and 7.4% for FSH, LH, estradiol, prolactin, 17-hydroxy-progesterone, DHEAS, TSH, total testosterone, free testosterone and insulin respectively.

Özer A., Bakacak M., Kıran H., Ercan Ö., Köstü B., Kanat-Pektaş M., Kılınç M, & Aslan F. (2016). Increased oxidative stress is associated with insulin resistance and infertility in polycystic ovary syndrome. Ginekologia polska, 87(11).

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Plasma Biochemical Analyses

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Commercial enzymatic tests were used to determine in plasma samples: glucose (GOD-PAP, Roche Diagnostics, Spain), triacylglycerides (LPL/GPO-Trinder Roche Diagnostics, Spain), glycerol (GPO-Trinder, Sigma Diagnostic, Spain), cholesterol (Menarini, Italy), non-esterified fatty acids (NEFA) (ACS-ACOD, Wako Chemicals GmbH, Germany) and ketone bodies (Wako Chemicals GmbH, Germany). Plasma insulin was determined with a specific EIA kit for rats (Mercodia, Denmark). Corticosterone, leptin and adiponectin were determined in plasma samples by X-Map Technology (Bioplex 100X, Spain) using the "rat stress hormone" RSH69K and "rat adipocyte" RADPCYT-82 panels (Millipore, Spain).

Limones M., Sevillano J., Sánchez-Alonso M.G., Herrera E, & Ramos-Álvarez M.D.P. (2019). Metabolic alterations associated with maternal undernutrition during the first half of gestation lead to a diabetogenic state in the rat. European journal of nutrition, 58(6).

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Diabetic Rat Model and Dgkh Overexpression

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The Central South University Department of Laboratory Animals provided healthy male Sprague–Dawley (SD) rats (180–200 g) that had been reared under specific-pathogen-free conditions. After 1 week of adaptive feeding, the rats were randomly separated into diabetes and normal control groups. STZ (55 mg/kg, Sigma, St. Louis, MO, USA) was administered intraperitoneally to SD rats in the diabetic group to cause diabetes [59 ]. The glucose oxidase method was used to measure fasting plasma glucose levels (GOD-PAP; Boehringer Mannheim). Following 3 days of STZ injection, rats with blood glucose levels greater than 16.7 mmol/l were chosen for follow-up investigations [60 (link)]. The normal control and diabetic groups were divided into four groups at random for ventricular stereotaxic injection after the induction of diabetes for 10 weeks: (1) control rats stereotaxically injected with negative adenovirus (CON + AD-NULL); (2) diabetic rats stereotaxically injected with negative adenovirus (DM + AD-NULL); (3) diabetic rats stereotaxically injected with overexpression of Dgkh adenovirus (DM + AD-Dgkh); and (4) control rats stereotaxically injected with overexpression of Dgkh adenovirus (CON + AD-Dgkh). Behavioral experiments were performed at week 12, and the rats were sacrificed after the behavioral experiments had been completed.

Qu M., Zuo L., Zhang M., Cheng P., Guo Z., Yang J., Li C, & Wu J. (2023). High glucose induces tau hyperphosphorylation in hippocampal neurons via inhibition of ALKBH5-mediated Dgkh m6A demethylation: a potential mechanism for diabetic cognitive dysfunction. Cell Death & Disease, 14(6), 385.

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