ArticleMolecular imaging and biology2014
Dexamethasone-induced insulin resistance: kinetic modeling using novel PET radiopharmaceutical 6-deoxy-6-[(18)F]fluoro-D-glucose.
Article in Molecular imaging and biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Empagliflozin attenuates dexamethasone-induced non-alcoholic steatohepatitis by regulation of ferroptosis, inflammation and autophagy.Frontiers in pharmacology · 2026Article
- Unraveling the Antihyperglycemic Effects of Dipeptyl Peptidase-4 Inhibitors in Rodents: A Multi-Faceted Approach Combining Effects on Glucose Homeostasis, Molecular Docking, and ADMET Profiling.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Determinants of Femur and Tibia Fragility in Diabetes Using Dexamethasone-Induced Insulin Resistance in Rats.Journal of diabetes research · 2025Article
- L-carnitine attenuates autophagic flux, apoptosis, and necroptosis in rats with dexamethasone-induced non-alcoholic steatohepatitis.BMC pharmacology & toxicology · 2024Article
- Dexamethasone-associated metabolic effects in male mice are partially caused by depletion of endogenous corticosterone.Frontiers in endocrinology · 2022Article
- Computational modeling of PET tracer distribution in solid tumors integrating microvasculature.BMC biotechnology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeAn insulin-resistant rat model, induced by dexamethasone, was used to evaluate a Michaelis-Menten-based kinetic model using 6-deoxy-6-[(18)F]fluoro-D-glucose (6-[(18)F]FDG) to quantify glucose transport with PET. PROCEDURES: Seventeen, male, Sprague-Dawley rats were studied in three groups: control (Ctrl), control + insulin (Ctrl + I), and dexamethasone + insulin (Dex + I). PET scans were acquired for 2 h under euglycemic conditions in the Ctrl group and under hyperinsulinemic-euglycemic conditions in the Ctrl + I and Dex + I groups.
resultsGlucose transport, assessed according to the 6-[(18)F]FDG concentration, was highest in skeletal muscle in the Ctrl + I, intermediate in the Dex + I, and lowest in the Ctrl group, while that in the brain was similar among the groups. Modeling analysis applied to the skeletal muscle uptake curves yielded values of parameters related to glucose transport that were greatest in the Ctrl + I group and increased to a lesser degree in the Dex + I group, compared to the Ctrl group.
conclusion6-[(18)F]FDG and the Michaelis-Menten-based model can be used to measure insulin-stimulated glucose transport under basal and an insulin resistant state in vivo.
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