Abstract
Patients with simple exogenous obesity are characterized by increased B-endorphin (B-EP) plasma levels, despite normal ACTH and B-Lipotropin (B-LPH). To evaluate the origin of such an hyperendorphinemia, 42 obese patients were submitted to a short overnight dexamethasone suppression test (DST: 1 mg at 23:00 h). Blood samples were taken in basal conditions and 9, and 17 h after DST. The same procedure was applied in 12 healthy, normal weight volunteers. In further five patients, 0.5 mg per 4/die were given. B-EP was measured by radioimmunoassay (RIA) after silicic acid extraction and Sephadex G-75 column chromatography. ACTH and Cortisol were measured by direct IRMA and RIA, respectively. Basal B-EP levels of patients (24.2 ± 16.5, fmol/ml, M ± SD) were double than in normal weight controls (10.8 ± 4.6), while ACTH and cortisol fell in the normal range. ACTH and cortisol were significantly reduced by DST in both patients and controls, while B-EP in patients did not. Cortisol, however, was not suppressed in 7 patients (16%). At 08:00, the suppression of B-EP in controls was 49.0 ± 18.4%, while in obese patients it was only 21.2 ± 38.8% (p < 0.01). However, patients with weight excess below 50% normally suppressed B-EP (41.6 ± 15.3%), while those with weight excess over 75% did not (11.3 ± 47.5%). The doubling of dexamethasone intake does not lead to a suppression of plasma B-EP in these last patients. These data indicate the existence of neuroendocrine abnormalities in the hypothalamus-pituitary-adrenal axis of obese patients and suggest that their hyperendorphinemia originates outside the anterior pituitary.
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Facchinetti, F., Giovannini, C., Petraglia, F. et al. Plasma B-endorphin resistance to dexamethasone suppression in obese patients. J Endocrinol Invest 11, 119–123 (1988). https://doi.org/10.1007/BF03350117
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DOI: https://doi.org/10.1007/BF03350117