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S Yang, X Xu, P Björntorp, and S Edén
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
C Nilsson, D Swolin-Eide, C Ohlsson, E Eriksson, HP Ho, P Bjorntorp, and A Holmang
Leptin is involved in regulating food intake, energy balance and bone formation. Increasing evidence suggests that leptin is also involved in fetal growth and development. The aim of this study was to determine if increased maternal leptin is followed by changes in body composition, skeletal growth or hormonal regulation in the adult rat offspring. Pregnant rats were given injections of either human recombinant leptin (3.5 mg/kg, i.p.) or vehicle on days 8, 10 and 12 of gestation. Both genders of leptin-exposed offspring showed significantly reduced adipose tIssue weight at adult age. Skeletal growth and cortical bone dimensions were significantly reduced. Circulating testosterone levels were significantly increased in female leptin-exposed offspring, and male leptin-exposed offspring had significant testicular enlargement. No significant effects were seen on circulating leptin levels or hypothalamic protein levels of the leptin receptor. The results demonstrate that maternally administered leptin is involved in fetal growth and development, leading to lean offspring with reduced skeletal growth.