Key result
Steroid diabetes mellitus rats exhibited increased skeletal muscle glucose uptake and compensatory insulin secretion, contrasting with decreased uptake and reduced insulin in type 2 diabetes mellitus rats.
Why the study?
The study was conducted to visualize glucose metabolism changes in main glucose-metabolizing organs and investigate the pathogenesis of steroid diabetes mellitus compared to type 2 diabetes mellitus using 18F-FDG PET/CT.
Does glucose metabolism in major organs differ between steroid diabetes mellitus and type 2 diabetes mellitus in rat models?
Does glucose metabolism in major organs differ between steroid diabetes mellitus and type 2 diabetes mellitus in rat models?
18F-FDG PET/CT imaging reveals that steroid diabetes mellitus differs from type 2 diabetes mellitus, showing increased skeletal muscle glucose uptake and compensatory insulin secretion rather than reduced uptake and beta-cell atrophy.
Answers are grounded in this paper and cite their sources.
Should not yet inform clinical steroid diabetes management; leaves open mechanistic distinctions from type 2 diabetes for human validation.
AIMS: F-FDG PET/CT can reflect the glucose metabolism of tissues and organs under living conditions. Here, PET/CT imaging of SDM and type 2 diabetes mellitus (T2DM) rats was used to visualize changes in glucose metabolism in the main glucose metabolizing organs and investigate the pathogenesis of SDM. METHODS: SDM 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. RESULTS: SDM 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. CONCLUSIONS: The 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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Zhao et al. (2020) studied Steroid diabetes mellitus and Type 2 diabetes mellitus (n=45). Dexamethasone vs. Normal saline was evaluated on Glucose uptake in skeletal muscle and liver (p=<0.01). Steroid diabetes mellitus rats exhibited increased skeletal muscle glucose uptake and compensatory insulin secretion, contrasting with decreased uptake and reduced insulin in type 2 diabetes mellitus rats.
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