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Jointly Amplified Basal and Pulsatile Growth Hormone (GH) Secretion and Increased Process Irregularity in Women with Anorexia Nervosa: Indirect Evidence for Disruption of Feedback Regulation within the GH-Insulin-Like Growth Factor I Axis¹

Department of Endocrinology (M) and Center for Eating Disorders, Odense University Hospital (R.K.S., J.H., J.K., C.H.), DK-5000 Odense, Denmark; the Department of Internal Medicine, National Science Foundation Center for Biological Timing, University of Virginia Health Sciences Center (J.D.V.), Charlottesville, Virginia 22908; Medical Department M (Endocrinology and Diabetes), Medical Research Laboratory and Institute of Experimental Clinical Research, University Hospital of Aarhus (A.F.), DK-8000 Aarhus, Denmark; the Department of Medical Physiology, Panum Institute, University of Copenhagen (J.V.), DK-2200 Copenhagen, Denmark; and the Department of Clinical Chemistry, Sonderborg Hospital (O.G.K.), DK-6400 Sonderborg, Denmark

Address all correspondence and requests for reprints to: René Klinkby Støving, M.D., Department of Endocrinology (M), Odense University Hospital, DK- 5000 Odense C, Denmark.

Anorexia nervosa (AN) is associated with multiple endocrine alterations. In the majority of AN patients, basal and GHRH-stimulated serum GH levels are increased. The metabolic effects of GH are known to be related to its pulsatile secretory pattern. The present study was performed to examine GH pulsatility in AN using the techniques of deconvolution analysis and approximate entropy, which quantify secretory activity and serial irregularity of underlying hormone release not reflected in peak occurrence or amplitudes. To this end, 24-h GH profiles were obtained by continuous blood sampling aliquoted at 20-min intervals in 8 nonfasting patients with AN [body mass index (BMI), 14.2 ± 0.8 kg/m²; mean ± SEM) and in 11 age-matched healthy women (BMI, 20.3 ± 0.5 kg/m²).

The deconvolution-estimated half-life of GH was not altered in the AN patients. The pituitary GH secretory burst frequency, burst mass, and burst duration were each significantly increased in women with AN compared to those in normal weight women. A 4-fold increase in daily pulsatile GH secretion was accompanied by a 20-fold increase in basal (nonpulsatile) GH secretion. There were significant negative correlations between BMI and the basal as well as pulsatile GH secretion rates. Moreover, AN patients exhibited significantly greater GH approximate entropy scores than the controls, denoting marked irregularity of the GH release process. In contrast to previous reports in healthy fasting subjects, cortisol levels in AN patients were positively correlated to GH secretion rates. Leptin levels were significantly inversely correlated to the pulsatile, but not the basal, GH secretion rate.

The present data demonstrate augmented basal as well as pulsatile GH secretion with disruption of the orderliness of the GH release process in AN. Accordingly, GH secretion in AN probably reflects altered neuroendocrine feedback regulation, e.g. associated with increased hypothalamic GHRH discharge superimposed on reduced hypothalamic somatostatinergic tone.

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