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Background: Simple surrogate indexes (SSI) to assess beta-cell function, insulin sensitivity (IS) and insulin resistance (IR) are an easy and economic tool used in clinical practice to identify glucose metabolism disturbances.
Aim: To evaluate the validity and reliability of SSI that estimate beta-cell function, IS and IR using as a reference the parameters obtained from the frequently sampled intravenous glucose tolerance test (FSIVGTT).
Material And Methods: We included 62 subjects aged 20-45 years, with a normal body mass index and without diabetes or prediabetes. SSI were compared with the acute insulin response to glucose (AIRg), insulin sensitivity index (Si) and disposition index (DI) obtained from the FSIVGTT using the minimal model approach. Half of the participants (n = 31) were randomly selected for a second visit two weeks later to evaluate the reliability of all the variables.
Results: HOMA1-%B and HOMA2-%B had a significant correlation with AIRg (Spearman Rho (rs) = 0.33 and 0.37 respectively, p < 0.01). The SSI evaluating IS/IR that showed stronger correlation (rs > 0.50) with Si were fasting insulin, HOMA1-IR, HOMA2-IR, HOMA1-%S, HOMA2-%S, QUICKI, and the McAuley index. The parameters that showed good reliability with an intraclass correlation coefficient (ICC) > 0.75 were AIRg, HOMA1-%S, HOMA2-%S, and QUICKI.
Conclusions: Our results suggest that most of the SSI are useful and reliable.
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http://dx.doi.org/10.4067/S0034-98872022001101458 | DOI Listing |
JCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFApoptosis
September 2025
State Key Laboratory of Resource Insects, Medical Research Institute, Southwest University, Chongqing, 400715, China.
Colorectal cancer (CRC) is one of the most common and lethal malignancies worldwide, with treatment failure often attributed to chemoresistance and evasion of apoptosis. Cathayanon E (CE), a natural chalcone derivative isolated from Morus alba, has shown anticancer potential, but its role and mechanism in CRC remain largely unexplored. In this study, CE significantly inhibited CRC cell proliferation and induced apoptosis both in vitro and in vivo.
View Article and Find Full Text PDFDiabetologia
September 2025
Walther Straub Institute of Pharmacology and Toxicology, LMU Munich, Munich, Germany.
Aims/hypothesis: Unimolecular peptides targeting the receptors for glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon (GCG) have been shown to improve glycaemic management in both mice and humans. Yet the identity of the downstream signalling events mediated by these peptides remain to be elucidated. Here, we aimed to assess the mechanisms by which a validated peptide triagonist for GLP-1/GIP/GCG receptors (IUB447) stimulates insulin secretion in murine pancreatic islets.
View Article and Find Full Text PDFDiabetologia
September 2025
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Aims/hypothesis: Alpha cell dysregulation is an integral part of type 2 diabetes pathophysiology, increasing fasting as well as postprandial glucose concentrations. Alpha cell dysregulation occurs in tandem with the development of insulin resistance and changes in beta cell function. Our aim was to investigate, using mathematical modelling, the role of alpha cell dysregulation in beta cell compensatory insulin secretion and subsequent failure in the progression from normoglycaemia to type 2 diabetes defined by ADA criteria.
View Article and Find Full Text PDFmBio
September 2025
Department of Biology, Laboratory of Molecular Cell Biology, KU Leuven, Leuven, Flanders, Belgium.
Echinocandins, which target the fungal β-1,3-glucan synthase (Fks), are essential for treating invasive fungal infections, yet resistance is increasingly reported. While resistance typically arises through mutations in Fks hotspots, emerging evidence suggests a contributing role of changes in membrane sterol composition due to mutations. Here, we present a clinical case of () in which combined mutations in and , but not alone, appear to confer echinocandin resistance.
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