Photoperiodic Control of Adipocyte α2-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 photopheriod with testosterone treatments (1mg/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+RT hamsters. Whatever the experimental conditions the adipocyte .beta.-AR receptivity (lipolytic response of isoproterenol and [125I]cyanopinolol binding), and the A1-R receptivity (antilipolytic response inhitiated by (-)phenylisopropyladenosine and [3H]dipropyl-8-cyclpentylxanthine 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 thephotoperiod by a testosterone-dependent mechanism probably mediated through the hypothalamic-pituitary axis, without any alteration of the animal fat stores.