ArticleActa diabetologica2020
The difference between steroid diabetes mellitus and type 2 diabetes mellitus: a whole-body
Article in Acta diabetologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Advanced Gene-Expression Analysis of Skeletal Muscles Focusing on Normal, Glucose-Intolerant, and Diabetic Individuals with Type 2 Diabetes.Biomedicines · 2025Article
- Gut-X Axis and Its Role in Poultry Bone Health: A Review.Microorganisms · 2025Review
- Pilot investigations into the mechanistic basis for adverse effects of glucocorticoids in dysferlinopathy.Skeletal muscle · 2024Article
- Harnessing dual-energy CT for glycogen quantification: a phantom analysis.Quantitative imaging in medicine and surgery · 2023Article
- Imaging in experimental models of diabetes.Acta diabetologica · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsSteroid diabetes mellitus (SDM) is a metabolic syndrome caused by an increase in glucocorticoids, and its pathogenesis is unclear.
methodsSDM and T2DM rat models were established. During this time, PET/CT imaging was used to measure the %ID/g value of skeletal muscle and liver to evaluate glucose uptake. The pancreatic, skeletal muscle and liver were analyzed by immunohistochemistry.
resultsSDM rats showed increased fasting blood glucose and insulin levels, hyperplasia of islet α and β cells, increased FDG uptake in skeletal muscle accompanied by an up-regulation of PI3Kp85α, IRS-1, and GLUT4, no significant changes in liver uptake, and that glycogen storage in the liver and skeletal muscle increased. T2DM rats showed atrophy of pancreatic islet β cells and decreased insulin levels, significantly reduced FDG uptake and glycogen storage in skeletal muscle and liver.
conclusionsThe pathogenesis of SDM is different from that of T2DM. The increased glucose metabolism of skeletal muscle may be related to the increased compensatory secretion of insulin. Glucocorticoids promote the proliferation of islet α cells and cause an increase in gluconeogenesis in the liver, which may cause increased blood glucose.
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