Spontaneous Nocturnal Growth Hormone Secretion in Anorexia Nervosa

Abstract

Abstract In anorexia nervosa, serum GH levels are increased under basal conditions and respond abnormally to provocative stimuli. We report here, for the first time, an analysis of pulsatile GH secretion in these patients performed by Cluster algorithm. Seven anorectic and six normal weight, healthy women underwent serial blood sampling at 20-min intervals from 2030–0830 h for GH estimation. The total area under the curve (AUC; micrograms per L/min) was elevated 4-fold in anorectic patients compared to controls (4743.0 ± 1520.09 vs. 1148.6 ± 519.27; P < 0.01), largely due to an increase in the nonpulsatile fraction (3212.5 ± 990.45 vs. 378.7 ± 123.27; P < 0.01). Accordingly, the valley mean value was higher in anorectic than in control subjects (5.9 ± 2.25 vs. 1.0 ± 1.30 μg/L; P < 0.01). Furthermore, pulsatile AUC was also greater in anorectic patients (1530.4 ± 654.72 vs. 769.8 ± 404.02; P < 0.01) due to a significant increase in GH peak frequency (5.0 ± 0.81 vs. 3.0 ± 0.89; P < 0.01). No correlations were observed in these patients between body mass index and any of the parameters of spontaneous GH release, whereas a positive correlation was found between insulin-like growth factor I levels and pulsatile AUC (r2 = 0.583; P < 0.05), peak height (r2 = 0.743; P = 0.01), peak increment (r2 = 0.801; P < 0.01), and GH valley mean (r2 = 0.576; P < 0.05). In conclusion, it appears that the enhanced GH secretion in anorexia nervosa is the result of an increased frequency of secretory pulses superimposed on enhanced tonic GH secretion. Although this latter is consistent with a reduction of hypothalamic SRIH tone, the former may be accounted for by an increased number of GHRH discharges. Considering that in normal weight and obese subjects parameters of GH release are negatively correlated with adiposity indexes, the lack of such a negative correlation in our patients suggests that the enhancement of spontaneous GH release in anorectic patients is not merely the consequence of malnutrition-dependent impairment of insulin-like growth factor I production, but reflects a more complex hypothalamic dysregulation of GH release.