Abstract
AimsSteroid diabetes mellitus (SDM) is a metabolic syndrome caused by an increase in glucocorticoids, and its pathogenesis is unclear. 18F-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.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.
Highlights
Glucocorticoids are of key clinical use, due to their effective anti-inflammatory, anti-allergic, and immunosuppressive effects [1]
18F-FDG PET imaging has been used to study the glucose metabolism of organs such as the liver, fat, skeletal muscle, and myocardium [17,18,19], and the results show that this approach allows for the effective evaluation of glucose uptake by these organs
The results showed that the levels of glucose transporter 4 (GLUT4) (P < 0.05), insulin receptor substrate 1 (IRS-1) (P < 0.0001), and PI3Kp85α (P < 0.001) mRNA in the skeletal muscle of steroid diabetes mellitus (SDM) rats were significantly higher than those of type 2 diabetes mellitus (T2DM) rats (Fig. 4c)
Summary
Glucocorticoids are of key clinical use, due to their effective anti-inflammatory, anti-allergic, and immunosuppressive effects [1]. Excessive glucocorticoids (endocrine corticosteroid secretion or exogenous glucocorticoid intake) in the body often leads to glucose metabolism disorders, a condition termed steroid diabetes mellitus (SDM). Domestic and foreign studies generally classify SDM as type 2 diabetes mellitus (T2DM). The previous studies have shown that both acute and chronic glucocorticoids exposure can inhibit insulin release in a dose-dependent manner in rodents [6, 7]. Van et al [8] found that after prednisolone treatment, there was an impaired glucose tolerance, reduced C peptide secretion stimulated by arginine, and islet cell
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