Glucose (C311 autoanalyzer, Roche, Mannheim, Germany) and insulin (cobas e11, Roche, Mannheim, Germany) were measured in plasma and the homeostatic model assessment (HOMA) was used to estimate insulin resistance (HOMA2-IR2; The Oxford Centre for Diabetes, Endocrinology and Metabolism, UK) [48 (link)]. As described previously [14 (link)], MOTS-c was extracted from plasma in acetonitrile-hydrochloric acid and measured using an in-house sandwich ELISA developed at the University of Southern California by the laboratory that first described MOTS-c in human and murine plasma. This ELISA has been extensively validated, and peptide blocking experiments have been undertaken to show specificity of the antibody [14 (link)].
C311 autoanalyzer
Manufactured by Roche
Sourced in Switzerland
The C311 autoanalyzer is a laboratory instrument designed for automated clinical chemistry analysis. It is capable of performing a variety of analytical tests on patient samples. The core function of the C311 autoanalyzer is to provide efficient and accurate results for clinical chemistry tests, enabling healthcare professionals to make informed decisions about patient care.
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Lab products found in correlation
6 protocols using c311 autoanalyzer
1
Quantification of Insulin Resistance and MOTS-c
2
Comprehensive Cardiometabolic Risk Assessment
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Pre-informed written consent was obtained from each participant before beginning data collection. The details of the data collection have been described previously (Prabhakaran et al., 2017 (link)). Detailed questionnaires were administered to collect data on socio-demographic factors, medical history, and lifestyle factors, including diet, physical activity, tobacco smoking, and alcohol consumption. Daily fat consumption (g/day) was estimated from the detailed food frequency questionnaire, and the physical activity scores were categorized. The physical measures included anthropometry for height, weight, and waist and hip girths, along with blood pressure measurements. Fasting blood samples were collected from the participants, and the time of the last meal was recorded. Serum and plasma samples were used for generating data on glycemic and lipid levels. Plasma glucose was measured using the hexokinase method, total cholesterol was estimated using the enzymatic cholesterol oxidase method, and HDL-C was assayed by a direct method using PEG-modified enzymes and dextran sulfate using kits from Roche Diagnostics, Switzerland, on the c311 autoanalyzer (Roche). LDL-C was estimated using the Friedewald equation (Friedewald et al., 1972 (link)).
3
Plasma Lipid and Apolipoprotein Profiling
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Plasma total and unesterified cholesterol, triglyceride and HDL-C levels were determined with standard enzymatic techniques; LDL-C was calculated with the Friedewald's equation. Plasma apolipoprotein levels were measured by immunoturbidimetry on a Roche c311 autoanalyzer. The plasma preβ-HDL content, expressed as percentage of total plasma apolipoprotein A-I (apoA-I), was determined by native 2-DE, in which agarose gel electrophoresis was followed by nondenaturing gel gradient electrophoresis (GGE), and subsequent immunoblotting for apoA-I [10] . Plasma LCAT concentration was measured by an immunoenzymatic assay [11] , and the esterification of cholesterol incorporated into an exogenous standardized substrate (LCAT activity) was measured as previously described [9] . Plasma haptoglobin levels were determined via enzyme-linked immunosorbent assay (ELISA) using the Human Haptoglobin Quantikine ELISA kit (catalogue #DHAPG0; R&D Systems, Inc., Minneapolis, USA) according to the manufacturer's instructions.
4
Plasma Biochemistry and Amino Acids Analysis
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Baseline blood biochemistry and the time course of plasma glucose levels were analysed using a Roche C311 autoanalyzer, (Roche, Mannheim, Germany) by enzymatic colorimetric assay. Plasma insulin concentrations were analysed using electrochemiluminescence immunoassay on Cobas e 411 (Roche, Mannheim, Germany). The homeostatic model assessment (HOMA) insulin resistance was calculated based as reported by Mathews et al. [29 (link)]. Plasma samples were deproteinised by tungstate precipitation and amino acid concentrations were measured using a fluorescent derivitisation utilising the reaction of amino nitrogen with 6-aminoquinolyl-N-hydroxysuccinimidyl carbonate and subsequent separation by ultra-high pressure liquid chromatography as previously described [30 (link)].
5
Comprehensive Lipid Profiling: A Standardized Approach
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Blood samples were collected after an overnight fast in Na2-EDTA tubes, plasma was separated by low-speed centrifugation at 4°C within a few minutes from collection, and then immediately frozen. Plasma total and HDL cholesterol, unesterified cholesterol (UC), triglyceride (TG), phospholipid (PL), and apolipoprotein levels were determined with certified methods using a Roche c311 autoanalyzer (Roche Diagnostics) (11 (link)). The amount of CEs was calculated by subtracting UC from total cholesterol, and the difference was multiplied by 1.68 to have a precise estimation of the CE mass. LDL and non-HDL cholesterol were calculated by the Friedewald’s equation and as the difference between total cholesterol and HDL-cholesterol, respectively. In the case of TG levels >400 mg/dl, LDL cholesterol was assessed using a direct measurement method. Plasma CE and PL FA composition (CEFA, PLFA) was measured by a gas-liquid chromatographic method (12 (link)) in a representative group of subjects. Profile of FAs in plasma TG (TGFA) was determined by LC-MS/MS as previously described (13 ). TG species were detected as neutral loss of one FA chain. FA distribution was determined from molecular mass, FA chain loss, and retention time. Hepatic and intestinal SOAT2 contribution to CE formation was evaluated by analyzing CEFA composition in VLDL and chylomicrons, respectively, as described below.
6
Muscle Damage Biomarker Quantification
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Blood serum samples were assayed for creatine kinase (CK) activity and myoglobin concentration as systemic markers of muscle damage using a Roche C311 autoanalyzer (Roche, Mannheim, Germany) by enzymatic colorimetric assay. Complete blood cell counts were performed on whole EDTA blood (1 ml) by LabPLUS (Auckland, New Zealand) to determine circulating leukocyte number using a Sysmex XN-10 hematology analyzer (Auckland, New Zealand). For isolation of PBMCs, whole EDTA blood (2 ml) was layered over 2 ml of Histopaque solution (Sigma-Aldrich, St. Louis, MO) and centrifuged for 30 min at 400 g at room temperature. PBMCs were aspirated from the upper layer interface, washed twice with phosphate buffered saline, and pelleted by centrifugation at 250 g for 10 min at room temperature. PBMC cell pellets were immediately homogenized with 600 l RLT plus RNA lysis buffer (Qiagen, Hilden, Germany), and then stored at Ϫ80°C until subsequent RNA extraction.
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