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ABSTRACT
Plasma concentrations of LH, FSH, prolactin and progesterone were measured during the oestrous cycle in obese (fa/fa) and non obese (Fa/?) Zucker rats. In obese rats the mid-afternoon surge of LH during prooestrus was reduced compared with that in non-obese rats (P<0.05), and the maximum concentrations of FSH and prolactin declined more slowly during oestrus. Progesterone concentrations were higher during most of the oestrous cycle in obese rats. Oestradiol and progestin receptors were measured in the hypothalamus of female Zucker rats. Lower concentrations of oestradiol receptors were found in the preoptic area of obese rats (P<0.05). Concentrations of oestradiol receptors in the medial basal hypothalamus were also lower in obese rats, though the difference was not statistically significant. Concentrations of progestin receptors were similar in both phenotypes in the preoptic area and media basal hypothalamus. It seems likely that the abnormalities in reproductive hormones and oestradiol receptors contribute to the infertility of obese female Zucker rats. The underlying mechanism has still to be determined.
Journal of Endocrinology (1989) 120, 331–336
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ABSTRACT
Androgen receptor (AR) concentrations were measured in the prostates and livers of the infertile congenitally obese male Zucker rat and their fertile non-obese litter-mates. In obese rats AR concentrations were significantly lower in both the liver (p<0.001) and the prostates (p<0.01) of the obese rats compared with the non-obese rats, despite similar plasma testosterone concentrations in both phenotypes. These findings suggest that a potential cause for the infertility observed in the obese Zucker rat is a reduced sensitivity of target tissues to circulating androgens.
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The plasma oestradiol-17β concentrations of obese and non-obese female Zucker rats have been measured in three phases of the oestrous cycle. The oestradiol concentrations of both phenotypes were similar, and changed normally with the oestrous cycle. The weights of the uteri also changed normally with the cycle. Plasma androgen concentrations in male Zucker rats have also been measured: the mean concentration was slightly but significantly lower in obese rats, and androgen-sensitive tissues were slightly reduced in weight. The oestradiol-17β concentrations in males of both phenotypes were similar. It seems unlikely that deficient plasma concentrations of gonadal hormones cause the infertility of obese rats of either sex.
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Congenitally obese Zucker rats showed greater food intake, less running in activity wheels and greater body weight and fat content than the normal phenotype. Their food intake, running and body weight did not change significantly with the phase of the oestrous cycle. Ovariectomy had no effect on these variables or on body composition. Oestradiol replacement had little effect. Zucker rats of normal weight, however, showed a normal pattern of responses to the oestrous cycle, ovariectomy and oestradiol administration. The central regulation of energy balance and body weight appear to be insensitive to oestrogens in the obese Zucker rat.
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Abstract
The inhibitory effects of catecholamines on rat myometrium mediated by β-adrenoceptors are modulated by ovarian steroids. Previously reported findings of radioligand binding studies on myometrial membranes have demonstrated changes in the numbers of β-adrenergic binding sites following ovarian steroid treatment. However, these changes were not accompanied by parallel functional changes. In the present study, we have investigated possible mechanisms of heterologous β-adrenoceptor regulation by ovarian steroids. Binding studies were performed on myometrial membrane and cytosolic preparations from rats which had been ovariectomized and subsequently received no hormonal treatment or had been treated with oestradiol, progesterone or combined oestradiol and progesterone. The β-adrenergic antagonist [125I]iodocyanopindolol and the unlabelled competing agonist, isoprenaline, were used in the present studies. Hormonal treatment had no effect on the concentration of β-adrenergic binding sites in the myometrium (i.e. the number of membrane-bound and cytosolic binding sites per mg protein). However, significant changes were found in the total number of binding sites; these were associated with the hormone-induced tissue hypertrophy. In myometrium from ovariectomized-alone rats, approximately 50% of β-adrenergic binding sites were present in the cytosolic fraction. Oestradiol treatment, either on its own or in combination with progesterone, resulted in the translocation of binding sites to the cell membrane. However, in the absence of progesterone only 33% of the membrane-bound binding sites bound the β-adrenergic agonist, isoprenaline, with a high affinity, suggesting that the majority of these membrane-bound binding sites represented non-functional β-adrenoceptors. Progesterone treatment resulted in a doubling in number of the high affinity membrane-bound receptors. As a result of our findings we propose that oestrogen and progesterone act together in regulating β-adrenoceptor function: it is proposed that oestrogens increase the number of β-adrenergic binding sites associated with the cell membrane while progesterone promotes the coupling of these binding sites to their effector mechanisms thus leading to an increase in the number of functional β-adrenoceptors.
Journal of Endocrinology (1995) 147, 303–309