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Features of Lipid Metabolism in Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
The reason for the development of insulin resistance still remains to be established completely. One can think of the existence of many mechanisms leading to the development of relative insulin insufficiency. They include (i) a change in the chemical structure of the insulin, (ii) disturbance of the transformation of proinsulin into insulin, (iii) the increased secretion of insulin antagonists into the blood (as noted previously), and (iv) the formation of antibodies to insulin or disorder of the function of the insulin receptors. There are currently little proofs of the disturbance of the chemical structure of insulin, and also of the change in the transformation of proinsulin into insulin.
Endocrinology, growth and puberty
Published in Rachel U Sidwell, Mike A Thomson, Concise Paediatrics, 2020
Rachel U Sidwell, Mike A Thomson
Insulin is produced by the pancreatic β-cells as proinsulin. Proinsulin is broken down into C peptide (biologically inert) and insulin during the secretory process. The insulin then travels in the portal circulation to the liver where it exerts its main action.
Fibrinolysis and Diabetes Mellitus
Published in Pia Glas-Greenwalt, Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Michael W. Mansfield, Peter J. Grant
Proinsulin is the prohormone from which C-peptide is cleaved to produce insulin. With the development of specific monoclonal antibody assays for insulin and its precursors, it has been recognized that the less specific insulin radioimmunoassays that have been in common use overestimate actual insulin concentration because of cross-reactivity with the insulin precursors (especially proinsulin and 32–33 split proinsulin).125 This is particularly important in type 2 diabetic patients, in whom proinsulin and split proinsulin may account for over 60% of total immunoreactive insulin.126,127 When allowing for this inaccuracy, it is argued that patients with type 2 diabetes have absolute hypoinsuhnemia rather than hyperinsulinemia in the presence of insulin resistance.128
Autophagy in peripheral blood mononuclear cells is associated with body fat percentage
Published in Archives of Physiology and Biochemistry, 2023
Fabiano T. Amorim, Roberto C. Nava, Kurt A. Escobar, Zidong Li, Anna M. Welch, Zachary J. Fennel, Zachary J. McKenna, Ann L. Gibson
Serum glucose and LDL cholesterol were analysed using a colorimetric method with a detection range between 0 and 67 mg/dL (Crystal Chem, Elk Grove Village, IL, #81696) and 1.7–250 mg/dL (Crystal Chem, Elk Grove Village, IL, #80069), respectively. Insulin and proinsulin were determined via enzyme-linked immunosorbent assay (ELISA) with a detection range between 0.9 and 220 mU/L (Crystal Chem, Elk Grove Village, IL, #90095) and 0.5 and 220 pmol/L (Crystal Chem, Elk Grove Village, IL, #90110). IR (HOMA1-IR = glucose (mmol)×insulin (μU/mL)÷22.5) was estimated from the fasting glucose and insulin concentrations (Matthews et al.1985). C-reactive protein was quantified via ELISA with a detection range between 10 and 10,000 ng/mL (Crystal Chem, Elk Grove Village, IL, #80955). Adiponectin, leptin, and resistin were also quantified via ELISA with a detection range between 2 and 10,000 ng/mL (Crystal Chem, Elk Grove Village, IL, #80571), 1 and 100 ng/mL (Crystal Chem, Elk Grove Village, IL, #80968), and 20 and 10,000 pg/mL (Crystal Chem, Elk Grove Village, IL, #80588), respectively. All procedures and measurements were performed following the manufacturer’s recommendations.
Gut-derived bacterial flagellin induces beta-cell inflammation and dysfunction
Published in Gut Microbes, 2022
Torsten P.M. Scheithauer, Hilde Herrema, Hongbing Yu, Guido J. Bakker, Maaike Winkelmeijer, Galina Soukhatcheva, Derek Dai, Caixia Ma, Stefan R. Havik, Manon Balvers, Mark Davids, Abraham S. Meijnikman, Ömrüm Aydin, Bert-Jan H. van den Born, Marc G. Besselink, Olivier R. Busch, Maurits de Brauw, Arnold van de Laar, Clara Belzer, Martin Stahl, Willem M. de Vos, Bruce A. Vallance, Max Nieuwdorp, C. Bruce Verchere, Daniël H. van Raalte
Insulin was measured in low glucose KRB, high glucose KRB and cell lysate from GSIS experiments with ALPCO mouse ultrasensitive insulin ELISA according to manufacturer's instructions. Concentrations were normalized to total protein content measured via QuantiProTM BCA Assay Kit. IL-6 concentrations were measured in cell supernatants via ELISA MAXTM Deluxe Set Mouse IL-6 and IL-6 human uncoated ELISA kit according to manufacturer's instructions. Proinsulin was measured with Mercodia Rat/Mouse Proinsulin ELISA (Schweden). Lysates or glucose media from GSIS experiments were used. Ratios were calculated by dividing proinsulin with insulin for each of the nine replicates. CRP and LBP were measured in serum according to the manufacturer’s instructions (HycultBiotech, NL).
Beta-cell failure in type 2 diabetes: mechanisms, markers, and clinical implications
Published in Postgraduate Medicine, 2020
When beta cells produce insulin, it is first secreted as proinsulin. C-peptide is a 31-amino acid polypeptide that connects the alpha and beta chains of proinsulin [58]. Upon removal of C-peptide from the proinsulin molecule, the alpha and beta chains become linked, and proinsulin turns into insulin. Thus, C-peptide and insulin are present in beta cells in equal amounts and are co-secreted into the portal vein in equimolar amounts. In contrast to insulin, C-peptide does not undergo hepatic degradation and is cleared entirely in peripheral tissues at a relatively constant rate. C-peptide has a substantially longer half-life than insulin (approximately 35 min vs. 3–5 min) [59,60]. Furthermore, in individuals who are receiving insulin therapy, insulin assays cannot distinguish endogenous and exogenous insulin, but the differential kinetics of C-peptide mean that peripheral plasma C-peptide concentrations can be used to accurately estimate insulin secretion.