| Objective:Steroid diabetes mellitus（SDM）is a metabolic syndrome caused by an increase in glucocorticoids（GCs）,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 immunohistochemical analysis was used to investigate the pathogenesis of SDM.Methods:The SDM model was established by intraperitoneal injection of dexamethasone to Wistar rats and the T2DM model was established by feeding GK rats with high fat.During this time,changes in blood glucose,insulin levels,and glucose tolerance tests were monitored.PET/CT imaging was used to measure the%ID/g value of skeletal muscle and liver to evaluate glucose uptake.The pancreatic isletαandβcells,the expression of GLUT4and insulin signaling pathway-related proteins in skeletal muscle,and the glycogen content in skeletal muscle and liver were analyzed by immunohistochemistry.Results:SDM and T2DM rat models were successfully established.SDM rats showed increased fasting blood glucose and insulin levels,hyperplasia of isletαandβcells,increased 18F-FDG uptake in skeletal muscle accompanied by an up-regulation of PI3Kp85α,IRS-1,and GLUT4,no significant changed in liver uptake,and that glycogen storage in the liver and skeletal muscle increased.T2DM rats showed atrophy of pancreatic isletβcells and decreased insulin levels,significantly reduced 18F-FDG uptake and glycogen storage in skeletal muscle and liver,and decreased IRS-1 expression in skeletal muscle.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 isletαcells and cause an increase in gluconeogenesis in the liver,which may cause increased blood glucose. |
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