Objective: To define the mathematical relationship between fructosamine levels and average glucose values. Subjects and methods: The study comprised laboratory data of 1,227 patients with type 1 or 2 diabetes mellitus. Fructosamine levels measured at the end of a 3-week period were compared against the average blood glucose levels of the previous 3 weeks. Average glucose levels were determined by the weighted average of the daily fasting capillary glucose results performed during the study period, and the plasma glucose measured in the same sample collected for fructosamine measurement. Results: In total, 9,450 glucose measurements were performed. Linear regression analysis between fructosamine levels and average glucose levels showed that for each 1.0 µmol/L increase in fructosamine level there was a 0.5 mg/dL increase in average glucose level, as estimated by the equation Mean glucose level = (0.5157 x Fructosamine) -20. The coefficient of determination (r2 = 0.353492, p < 0.006881) allowed the calculation of the estimated average glucose based on fructosamine level. Conclusion: Our study demonstrated a linear correlation between fructosamine level and mean blood glucose level, suggesting that fructosamine levels can be a proxy for the average glucose level in assessing the metabolic control of patients with diabetes.
The history of muscle biopsy dates back to 1860, when Duchenne first performed a biopsy on a patient with symptoms of myopathy (1) . Since then, the basic and clinical science of muscle and muscle disease has gone through three stages of development: the classical period, the modern stage and the molecular era.
Objective To evaluate the possible similarity between the AA sequences of human insulin and human glutamic acid decarboxylase-65 (GAD65) with the SARS-CoV-2/COVID proteins to explain the possible trigger of DM1. Methods AA sequences of human insulin, GAD65 and SARS-CoV-2 were obtained from the Protein Data Bank archive information database (RCSB PDB). NetMHCpan v4.1 was used for epitope prediction. Sequences were compared using BLAST for epitope comparison and Pairwise Structure Alignment to assess protein similarity. The AA sequences of human insulin (4F0N) and GAD65 (2OKK) were compared with the sequences of the following SARS-CoV-2 proteins: SARS-Cov2 S protein at open state (7DDN), SARS-Cov2 S protein at close state (7DDD), SARS CoV-2 Spike protein (6ZB5), Crystal structure of SARS-CoV-2 nucleocapsid protein N-terminal RNA binding domain (6M3M), Crystal structure of SARS-CoV-2 nucleocapsid protein C-terminal RNA binding domain (7DE1), Crystal structure of NSP1 from SARS-CoV-2 (7K3N), and SARS-CoV-2 S trimer (7DK3)). Results The percent similarity between epitopes ranged from 45 to 60% (P 0.048) between both human insulin and SARS-CoV2 and for GAD 65 and SARS-CoV2, while the AA similarity of the evaluated samples ranged from 5.00–45.45% between human insulin and SARS-CoV2 and from 10.45–22.22% between GAD65 and SARS-CoV2. Conclusion Immunoinformatics data suggest a potential pathogenic link between SARS-CoV-2/COVID and DM1. Thus, by molecular mimicry, we found that sequence similarity between epitopes and AA sequence between SARS-CoV-2 / COVID and human insulin and GAD65 could lead to the production of an immune cross-response to self-antigens, with self-tolerance breakdown, which could thus trigger DM1.
Bile acids (BAs) are steroid molecules that have a hydrophilic and a hydrophobic end, and are synthesized exclusively in the liver, being end product of cholesterol catabolism. Type 2 diabetes mellitus (DM2) is a chronic degenerative disease, with a pathophysiology characterized by insulin resistance (IR), insulin deficiency due to insufficient production of pancreatic ß-cells, and elevated serum glucose levels leading to multiple complications. BAs are related to several metabolic alterations, including metabolic syndrome and DM2. It is currently known that BAs act as a ligand for the nuclear farnesoid X receptor, a receptor with an important role in glucose metabolism, lipids and cellular energy production, as well as in the regulation of production, elimination and mobilization of BAs. BAs have also been reported to act as a signaling pathway through of Takeda G protein-coupled receptor 5. In this manuscript, we describe the interface between BAs and metabolic disorders, in particular DM2, including discussing possibilities in the development of therapeutic procedures targeting BAs as an optional pathway in the treatment of DM2.
Introduction: Complexes of monomeric hormone molecules immunoglobulin-associated lead to the formation of macro-complexes biologically inactive that are called macro-hormones. Patients’ presenting unexpectedly elevated hormones values indicates the need that the existence of macro-hormones must be researched. Objective: To describe the macro-hormones discovered incidentally in laboratory tests, which we refer to as "incidentalormones". Methods: An integrative review was conducted, and data was gathered from the published articles in medical database. The different forms of macro-hormones are reviewed; the biochemical significance and laboratory assays of macro-hormones are also revised within the ambit of current laboratory medicine. We discussed diagnostic difficulty encountered in patients with "incidentalormones”, as well as methods of macro-hormone detection, immunoglobulin involved, clinical significance and associations with other diseases. Conclusion: The presence of macro-hormones, often guides us to intervention in laboratory trials, and could result in false-positive diagnosis with inadequate therapy. Laboratories should follow a diagnostic algorithm to carefully recognize and examine possible immunoassay interferences.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.