title: beta-Endorphin and adrenocortical function in obesity.
abstract: OBJECTIVE
  To test the hypothesis that the hyperendorphinaemia in obesity originates from outside the pituitary.
  
  
  METHODS
  Intravenous administration of corticotrophin-releasing hormone (CRH) after overnight suppression with 2 mg of dexamethasone in normal-weight controls and in obese subjects before and after weight reduction.
  
  
  METHODS
  Eleven obese females, age (mean +/- SEM) 30 +/- 2.1 years, body mass index (BMI) 41.2 +/- 1.9 kg/m2. Eight normal-weight females served as controls, age 26 +/- 2.1 years, BMI 21.4 +/- 0.5 kg/m2. Five obese subjects were also studied after weight loss of 18.4 +/- 1.0% of original weight.
  
  
  METHODS
  Plasma beta-endorphin, ACTH and cortisol. Cortisol production rate in 24-hour urine. Basal (without dexamethasone suppression) plasma beta-endorphin levels.
  
  
  RESULTS
  Basal (without dexamethasone suppression) beta-endorphin levels were 7.7 +/- 0.8 pmol/l in the obese and 3.8 +/- 0.5 pmol/l in the control subjects (P less than 0.005). The degree of suppression of beta-endorphin after dexamethasone was similar in the obese (23.2 +/- 3.7%) and in the control subjects (28.2 +/- 0.12%). Administration of CRH following dexamethasone suppression resulted in a small but significant increase of plasma beta-endorphin in both obese (from 1.55 +/- 0.12 to 2.32 +/- 0.28 pmol/l) and control subjects (from 0.98 +/- 0.24 to 1.69 +/- 0.33 pmol/l). The groups did not differ regarding this response, nor regarding the release of ACTH and cortisol after CRH. Cortisol production rate was higher (P less than 0.001) in the obese (68.7 +/- 3.3 mumol/24 h) than in the controls (40.0 +/- 3.0 mumol/24 h). No correlation between cortisol production rate and basal beta-endorphin levels was found. Weight loss appeared to have no influence on cortisol production rate, basal beta-endorphin levels, or on the responses to dexamethasone or CRH.
  
  
  CONCLUSIONS
  Plasma beta-endorphin in obese subjects can be affected by manipulations of the hypothalamic-pituitary-adrenocortical axis; the hypothesis that the hyperendorphinaemia of obesity originates from outside the pituitary cannot be confirmed.
authors.affiliation: Department of Endocrinology, University Hospital, Utrecht, The Netherlands.
authors.forename: P M
authors.initials: PM
authors.lastname: Zelissen
authors.forename: H P
authors.initials: HP
authors.lastname: Koppeschaar
authors.forename: D W
authors.initials: DW
authors.lastname: Erkelens
authors.forename: J H
authors.initials: JH
authors.lastname: Thijssen
mesh_terms: D000328:Adult; D003346:Corticotropin-Releasing Hormone; D003907:Dexamethasone; D005260:Female; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D009765:Obesity / Q000097:blood* / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D015431:Weight Loss / Q000502:physiology; D001615:beta-Endorphin / Q000097:blood*
chemical_list: D001615:beta-Endorphin; D003907:Dexamethasone; D003346:Corticotropin-Releasing Hormone