Session: SAT 1-25-Glucocorticoid Actions & HPA Axis
Poster Board SAT-24
The cortisol response to oral glucose load in PCOS and metabolic syndrome is not well understood. Decreased cortisol release after OGTT has been noted in obese subjects, which correlated with degree of insulin resistance and obesity. We believe that glucocorticoid (GC) sensitivity is associated with cortisol response in OGTT, as shown in comparison to in vitro GC binding assay.
We recruited 15 patients, 12 females with PCOS and 3 males with metabolic syndrome. GC sensitivity was evaluated by F-Dex binding assays. GC index (GCI) was calculated as area under curve (AUC) (Normal value 300 ±40, calculated from 12 control patients). A lower GCI represents decreased level of GC sensitivity. A 2-hour OGTT was performed on same patients where serum cortisol levels were obtained at 30-minute intervals. Cortisol index (CI) was calculated as AUC.
A positive correlation between GCI and CI was noted, indicating that lower GC sensitivity in a patient, the less of a cortisol response to OGTT and lower AUC (R=0.77, p<0.0001). Cortisol response was statistically different between GC sensitivity groups at 60, 90, and 120 minutes (Serum cortisol (mcg/dl): GC resistant patients at 60’ 11 ± 4.5, 90’ 7 ± 1.9, 120’ 7 ± 1.6; GC Sensitive patients at 60’ 21 ±10, 22 ± 12, 12 ± 6)
Low cortisol response during OGTT was associated with increased GC resistance. One suggested model can be cortisol metabolism enzymes such 11β-HSD1 in hepatocytes, which regulates glucose metabolism.
Nothing to Disclose: AP, DK, SP, APSB, SNG, SBT
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