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J Clin Endocrinol Metab. 1989 Mar;68(3):517-22.

Alterations of the adrenocorticotropin-cortisol axis in normal weight bulimic women: evidence for a central mechanism.

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Department of Reproductive Medicine, School of Medicine, University of California-San Diego, La Jolla 92093.


We studied pituitary-adrenal function in eight women with normal weight bulimia and seven normal women by measuring plasma ACTH and serum cortisol levels at 20-min intervals for 24 h and the responses to human CRH (hCRH) and to a noon meal. The bulimic women had increased 24-h transverse mean plasma ACTH [1.09 +/- 0.06 (+/- SE) vs. 0.75 +/- 0.14 pmol/L; P less than 0.05] and serum cortisol (235 +/- 21 vs. 152 +/- 9 nmol/L; P less than 0.005) concentrations. While the 24-h ACTH and cortisol pulse frequencies were unaltered, the bulimic women had higher (P less than 0.05) mean peak ACTH (1.46 +/- 0.09 vs. 1.03 +/- 0.15 pmol/L) and cortisol values (331 +/- 33 vs. 239 +/- 17 nmol/L). Despite having higher mean and peak plasma ACTH and serum cortisol values, the bulimic women had a blunted response of both ACTH (P less than 0.001) and cortisol (P less than 0.005) to hCRH, which included a lower mean maximal plasma ACTH response, decreased (P less than 0.05) integrated area under the ACTH response curve (161 +/- 12 vs. 231 +/- 23 pmol/min.L), a lower (P less than 0.05) maximum cortisol response (284 +/- 35 vs. 413 +/- 19 nmol/L), and decreased (P less than 0.05) area under the cortisol curve (11.1 +/- 1.9 vs. 15.9 +/- 1.3 X 10(3) nmol/min.L). The circadian variations of both ACTH and cortisol were maintained in the bulimic women; the nadir and acrophase times were similar to those of the normal women. However, the rise in serum cortisol that occurred within 1 h after the lunch meal in the normal women (104 +/- 35 nmol) did not occur in the bulimic women (P less than 0.05). These data demonstrate that marked changes in hypothalamic-pituitary-adrenal function occur in bulimia in the absence of weight disturbance and suggest central activation of CRH and/or synergistic factors as well as alterations in signals from gut to brain in this syndrome.

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