The effects of growth hormone (GH) and testosterone, alone or in combination, on the regulation of lipolysis in isolated adipocytes from hypophysectomized rats were investigated. Male Sprague-Dawley rats were hypophysectomized at 50 days of age. One week after operation, hormonal replacement therapy with l-thyroxine and hydrocortisone acetate was given to hypophysectomized rats. Groups of rats were treated with GH (1·33 mg/kg, daily), testosterone (10 mg/kg, once) alone or in combination. After one week of hormonal treatment, adipocytes were isolated from the pooled epididymal and perirenal fat pads and glycerol release after isoproterenol stimulation and 125I-cyanopindolol binding was measured. Hypophysectomy caused a marked decrease in basal and isoproterenol-stimulated lipolysis. There was no effect of testosterone treatment alone on lipolysis, but GH treatment resulted in an increase in isoproterenol-induced lipolysis but not to the levels observed in cells from control rats. Testosterone and GH in combination restored the lipolytic response to isoproterenol. Also 125I-cyanopindolol binding was decreased after hypophysectomy. Testosterone treatment alone and GH treatment alone increased the binding, while in combination the treatment had an additive effect. Affinity was not changed, but the effects seemed to be on receptor number, as determined by Scatchard analysis.
Forskolin-stimulated cAMP accumulation in adipocytes was markedly reduced after hypophysectomy. Testosterone treatment alone had no effect. GH treatment alone increased forskolin-stimulated cAMP accumulation, although the level was lower than that found in control rats. The combined treatment resulted in a further increase to levels observed in adipocytes from control rats.
These results demonstrate that GH and testosterone have additive effects in the regulation of lipolysis. Both hormones increase the β-adrenergic receptor density, partly explaining this additive effect. Moreover, GH may contribute to the lipolytic response by affecting steps distal to the receptor in the lipolytic cascade.
Journal of Endocrinology (1995) 147, 147–152