title: Oestradiol and progesterone change beta3-adrenergic receptor affinity and density in brown adipocytes.
abstract: OBJECTIVE
  To check if the oestradiol- and progesterone-driven reduction in noradrenaline responsiveness of brown adipocytes is due to a reduction in either the density or the affinity of beta3-adrenoceptors (beta3-AR). beta1/beta2-AR were also studied.
  
  
  METHODS
  Four groups of animals were considered. (i) control rats at thermoneutrality, (ii) cold-acclimated rats, to determine beta-AR under continuous sympathetic stimulation, which is known to decrease noradrenaline responsiveness, (iii) oestradiol- and (iv) progesterone-treated cold-acclimated rats to determine hormonal effects on beta-AR populations in thermogenically active brown adipocytes.
  
  
  METHODS
  Oestradiol and progesterone were chronically elevated by means of s.c. Silastic implants. Densities and affinities of beta-AR populations were determined by binding studies using [3H]CGP-12177 as radioligand.
  
  
  RESULTS
  Two populations of low and high binding affinities (K(d) 1.6 and 27.3 nmol/l) corresponding to beta3- and beta1/beta2-AR respectively were found at thermoneutrality. beta3-AR density was higher than that of beta1/beta2-AR (B(max) 419 and 143 fmol/mg protein respectively). Cold-acclimated rats showed a reduction of beta3-AR binding capacity (B(max) 308 fmol/mg protein). Oestradiol and progesterone reduced the density of beta3-AR to 167 and 185 fmol/mg protein respectively, while increasing their affinity for [3H]CGP-12177 (K(d) 9.5 and 4.0 nmol/l vs 16 nmol/l in cold-acclimated untreated rats). The density of beta1/beta2-AR was also reduced after oestradiol treatment (B(max) 51 fmol/mg protein).
  
  
  CONCLUSIONS
  Both oestradiol and progesterone reduce the density of beta3-AR in brown adipose tissue (BAT) while increasing their affinity for [3H]CGP-12177. Oestradiol also reduces the density of beta1/beta2-AR whereas cold-acclimation reduces the density of beta3-AR.
authors: Department of Animal Biology II (Physiology), Faculty of Biological Sciences, Complutense University, Madrid, Spain.
authors: A
authors: A
authors: Malo
authors: M
authors: M
authors: Puerta
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000187:drug effects* / Q000378:metabolism; D058673:Adrenergic beta-3 Receptor Antagonists; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001665:Binding Sites; D001667:Binding, Competitive; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D003080:Cold Temperature; D004958:Estradiol / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D009638:Norepinephrine / Q000037:antagonists & inhibitors; D011374:Progesterone / Q000008:administration & dosage / Q000494:pharmacology*; D011412:Propanolamines / Q000378:metabolism / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism*; D018709:Statistics, Nonparametric
chemical_list: D058673:Adrenergic beta-3 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D022702:Receptors, Adrenergic, beta-3; D011374:Progesterone; D004958:Estradiol; D011433:Propranolol; C033394:CGP 12177; D009638:Norepinephrine