Monica Shah 1, May M Adel 1, Bettina Tahsin 1, Yannis Guerra 1, Leon Fogelfeld 1
Main idea: Contrary to the assumption that insulin resistance is the main driver of glucocorticoid-induced hyperglycemia, results indicate that decreased beta-cell insulin secretion is the more likely cause in those with T2DM. These results may be caused by increased beta-cell fragility along with reduced recovery ability after glucocorticoid exposure.
Objective: For those with type 2 diabetes mellitus (T2DM), impact of short-term high-dose glucocorticoid exposure on beta-cell function is unknown. This study aims to compare the impact on beta-cell function and insulin resistance of prednisone 40 mg between adults with newly diagnosed T2DM and healthy adults.
Methods: Five adults with T2DM and five healthy adults were enrolled. Intervention therapy was prednisone 40mg daily for 3 days. Pre- and post-therapy testing included 75-g oral glucose tolerance, plasma glucose, C-peptide, and insulin.
Results: Upon therapy completion, HOMA-IR did not increase or differ between groups. Percentile difference for HOMA-%B and insulinogenic index in those with T2DM was significantly lower statistically (50.4% and 69.2% respectively) compared to healthy subjects (19% and 32.2%).