Session: SUN 690-701-Obesity Pathophysiology
Poster Board SUN-697
Goals: To characterize the relationship between basal and dynamic cortisol response to an intravenous bolus dose of 1 ug ACTH in obesity.
Methods: Total, free and salivary cortisol were tested at the basal state and after a standard challenge with 1 ug ACTH in 22 healthy obese subjects (mean BMI= 42) and 17 healthy lean controls (mean BMI=22).
Results: Mean (+/-SD) basal state total cortisol was significantly lower in obese than in lean subjects (11.7+/-3.6 vs. 15.5+/- 4.4 ug/dl, p=0.006) as were also basal state serum free cortisol (0.53+/-0.24 vs 0.76+/-0.36 ug/dl, p=0.004) and basal statesalivary cortisol (0.23+/-0.10 vs. 0.56+/-0.66 ug/dl, p=0.004). Additionally, baseline total cortisol was inversely related to BMI (r= -0.45; p<0.05), to waist circumference (r= -0.49; p<0.05) and to systolic blood pressure (r= -0.39; p<0.05). Upon challenge with 1ug ACTH, total cortisol response as assessed by either repeated measure ANOVA (p=0.019) or area under the response curve ((P=0.028) was also lower in obese than in lean subjects. Concordant with these findings peak post-1ug ACTH salivary cortisol was lower in the obese relative to the lean subjects (1.14 +/- 0.10 vs. 1.65+/- 0.66 ug/dl, p<0.05)
Conclusion: Basal state as well as peak stimulated cortisol and integrated post-1ug ACTH-stimulated total serum cortisol levels, while within the test-defined normal range, were significantly lower in obese subjects. Obesity is not associated with higher basal cortisol or ACTH-stimulated cortisol reserve and indeed is linked to diminished circulating cortisol which is negatively related to body mass index and waist circumference. In fact, increased serum or salivary cortisol is atypical for obesity and should not be viewed as probable "pseudo-Cushing syndrome".
Nothing to Disclose: YS, EO, YM, YG, GS, YM, SS, MY, RL, KMT, NS
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