title: Photoperiodic control of adipocyte alpha 2-adrenoceptors in Syrian hamsters: role of testosterone.
abstract: The impact of photoperiodic manipulations and testosterone treatments on the adipocyte alpha 2-adrenergic (alpha 2-AR), beta-adrenergic (beta-AR), and A1-adenosine (A1-R) responsiveness, was explored in male Syrian hamsters (Mesocricetus auratus). Moreover, binding studies were performed with appropriate alpha 2-AR, beta-AR, and A1-R radioligands to study receptor changes. Animals were kept for 12 weeks in long day photoperiod (LD: 16 h light (L)-8 h dark (D)), in short day photoperiod (SD: 6L-18D), or in short photoperiod with testosterone treatments (1 mg/animal/day sc) 10 days before sacrifice (SD+T). The antilipolytic effect of the full alpha 2-AR agonist UK14304 and the specific binding of the alpha 2-AR radioligands [3H] RX821002 (antagonist) and [3H]UK14304 were significantly reduced in SD hamsters compared with LD hamsters. The alpha 2-site number and alpha 2-AR responsiveness were completely restored in SD+T hamsters. Whatever the experimental conditions the adipocyte beta-AR receptivity (lipolytic response of isoproterenol and [125I]cyanopindolol binding), and the A1-R receptivity (antilipolytic response initiated by (-)phenylisopropyladenosine and [3H]dipropyl-8-cyclopentylxanthine and [3H]phenylisopropyladenosine binding) remained unchanged. Moreover, the kidney and brain alpha 2-AR densities identified with [3H]RX821002 were not significantly different in LD, SD or SD+T hamsters. These results were obtained without any modification of animal weight, white adipose tissue weight, or white fat cell size. We conclude that, in the Syrian hamster, the expression of the adipocyte alpha 2-AR is under the control of the photoperiod by a testosterone-dependent mechanism probably mediated through the hypothalamic-pituitary axis, without any alteration of the animal fat stores.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale (I.N.S.E.R.M. U.317), Université Paul Sabatier, Toulouse, France.
authors.forename: J S
authors.initials: JS
authors.lastname: Saulnier-Blache
authors.forename: D
authors.initials: D
authors.lastname: Larrouy
authors.forename: C
authors.initials: C
authors.lastname: Carpéné
authors.forename: N
authors.initials: N
authors.lastname: Quideau
authors.forename: M
authors.initials: M
authors.lastname: Dauzats
authors.forename: M
authors.initials: M
authors.lastname: Lafontan
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000316:Adrenergic alpha-Agonists / Q000378:metabolism / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism; D000068438:Brimonidine Tartrate; D006224:Cricetinae; D004146:Dioxanes / Q000378:metabolism; D019329:Idazoxan / Q000031:analogs & derivatives; D007545:Isoproterenol / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism; D008027:Light; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D008647:Mesocricetus; D010507:Periodicity; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011810:Quinoxalines / Q000378:metabolism / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000378:metabolism*; D013739:Testosterone / Q000494:pharmacology*
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004146:Dioxanes; D011810:Quinoxalines; D011942:Receptors, Adrenergic, alpha; D013739:Testosterone; C047975:cyanopindolol; D000068438:Brimonidine Tartrate; D010869:Pindolol; C058525:2-methoxyidazoxan; D007545:Isoproterenol; D019329:Idazoxan