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Biomedical subjects

F Naftolin

Publications and source records attributed to F Naftolin.

At least 307 records · Page 17Linked to original sources
PubMed1977

Pubertal food intake, body length, weight, and composition in the well fed female rat.

Pubertal age, food intake, body length, weight, and composition were determined by direct measurements in 29 well fed female rats studied from birth to first estrus. The average birth and weaning weights of the 12 early maturing rats were 6.99 +/- 0.13 g and 50.13 +/- 1.16 g, respectively, and did not differ significantly from those of the 11 late maturers (6.97 +/- 0.16 g and 49.72 +/- 1.42 g, respectively). Mean values for all pubertal measurements are included in Table 1. At puberty, the late maturing animals were heavier, longer, and had attained a greater quantity of total body water than the early maturers. Although both groups ate the same total amounts of food, late maturing rats at vaginal opening and at first estrus consumed relatively less food per 100 g body weight than did early maturers. Estrus was simultaneous with vaginal opening in 10 (83%) of early and 4 (36%) of the late maturing rats. Despite the similarity in the proportions of total body water, fat, and protein in early and late maturers, a regression analysis, shown in Figure 1, indicates a significant decrease in the proportion of body water (P less than 0.001), and a significant increase in the proportion of body fat (P less than 0.05) with increasing age at first estrus. The percentage of body protein does not change with increasing age at first estrus (regression coefficient = 0.13).

Animals↗
PubMed1977

Ineffectiveness of pyridoxine (B6) to alter secretion of growth hormone and prolactin and absence of therapeutic effects on galactorrhea-amenorrhea syndromes.

The acute effect of pyridoxine (B6) on serum GH and PRL levels and its chronic effects on galactorrhea in nine subjects (group I, n=4, idiopathic galactorrhea with normal PRL levels and normal menses; Group II, n=5, galactorrhea-amenorrhea with increased PRL levels) have been studied. Pyridoxine did not acutely alter GH or PRL levels. There was no decrease in galactorrhea, no resumption of menses and no decrease in PRL following tow months of B6 therapy. In contrast, bromocriptine was effective in suppressing galactorrhea and restoring normal menses in group II subjects and remains the therapy of choice for this purpose.

Amenorrhea↗
PubMed1976

Induction of menstruation with bromocryptine in patients with euprolactinemic amenorrhea.

Three nulliparous women presented with secondary amenorrhea with no evidence of endocrinopathy and normal skull x-ray. Pulsatile gonadotropin secretion was reduced, but an adequate pituitary gonadotropin reserve was demonstrable with luteinizing hormone-release factor provocation. The administration of bromocryptine was associated with amplification of pulsatile secretion of gonadotropins and was followed, in two of the three, by ovulatory menstruation. It is suggested that bromocryptine should be considered for induction of menstruation in euprolactinemic secondary amenorrhea.

Adult↗
PubMed1976

Serum luteinizing hormone, follicle-stimulating hormone, and testosterone responses to gonadotropin-releasing factor in males with varicoceles.

Five infertile males, ages 25 to 35, with oligospermia and varicocele had following gonadotropin-releasing hormone (LRF) infusion a rise of serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels which was not different from that of normal fertile males. The response of these hormones to LRF infusion was unaltered by spermatic vein ligation, but a significant elevation of the sperm count occurred. Thus, improvement in sperm count following spermatic vein ligation is not mediated via changes in peripheral gonadotropin or testosterone concentrations.

Adult↗
PubMed1976

Characterization of the inappropriate gonadotropin secretion in polycystic ovary syndrome.

To evaluate gonadotropin release in polycystic ovary syndrome (PCO), one or more of the following hypothalamic-pituitary function tests were performed on 24 patients with the syndrome. These tests included (a) the pulsatile pattern and day-to-day fluctuation of gonadotropin release; (b) effects of exogenous estrogen and antiestrogen (clomiphene) administration on gonadotropin release; and (c) pituitary responsiveness to maximal (150 mug) and submaximal (10 mug) luteinizing hormone-releasing factor (LRF) injections. In 10 of the 14 patients sampled frequently (15 min) for 6 h, luteinizing hormone (LH) levels were elevated above the concentration seen in normal cycling women (except the LH surge). These high LH concentrations appeared to be maintained by and temporally related to the presence of exaggerated pulsatile LH release, either in the form of enhanced amplitude or increased frequency. In all subjects, levels of follicle-stimulating hormone (FSH) were low or low normal, and a pulsatile pattern was not discernible. In four patients, daily sampling revealed marked day-to-day fluctuation of LH but not FSH. That the elevated LH levels were not related to a defect in the negative-feedback effect of estrogen was suggested by the appropriate fall of LH in four patients given an acute intravenous infusion of 17beta-estradiol. This infusion had no effect on FSH levels. In addition, clomiphene elicited rises of both LH and FSH that were comparable to the ones observed in normal women given the same treatment. The clomiphene study also suggested that the positive-feed-back mechanism of estrogen on LH release was intact when the preovulatory rises of 17beta-estradiol induced appropriate LH surges. The elevated LH levels appeared to be related to a heightened pituitary responsiveness to the LRF. This was found in the 11 and 2 patients given maximal (150 mug) and submaximal (10 mug) doses of LRF, respectively. The augmented pituitary sensitivity for LH release correlated with the basal levels of both estrone (P less than 0.025) and 17beta-estradiol (P less than 0.02). The net increase in FSH was significantly greater (P less than 0.001) in the PCO patients than the normal women with maximal doses of LRF. With the smaller dose study none of the injections had a discernible effect on FSH concentrations in either subject. The disparity between LH and FSH secretion could be explained by the preferential inhibitory action of estrogen on FSH release, coupled with a relative insensitivity of FSH release. These data indicate that in these PCO patients the abnormalities of the hypothalamic-pituitary regulation of gonadotropin secretion was not an inherent defect but represented a functional derangement consequent to inappropriate estrogen feedback, which led to a vicious cycle of chronic anovulation and inappropriate gonadotropin secretion.

Adult↗
PubMed1976

Catechol estrogen formation by the human fetal brain and pituitary.

Homogenates of central neuroendocrine tissues from 2 male and 1 female midtrimester fetuses were incubated with (23H) estradiol-17beta. Metabolism at the C-2 position was monitored by measuring the tritium incorporated into water in the incubate. Liberation of tritium from the substrate by hypothalamus, limbic tissues, parietal cortex and pituitary occurred to the extent of 5.1-12.7%, 1.6-8.5%, 4.7-10.8%, and 0.9-4.1% of starting radioactivity, respectively. The nature of the product was confirmed by the isolation of 14C labelled 2-hydroxyestrone derivative from separate incubations with 14C-estrone as the substrate. With or without correction for weight of tissue incubated, catechol estrogen formation under these conditions occurs at levels similar to those seen in rat brain homogenates except that in contrast to the rat, the human cortex is also highly active.

Brain↗
PubMed1976

Galactorrhea-amenorrhea syndromes: etiology and treatment.

Fifteen patients with galactorrhea-amenorrhea syndromes were studied before, during, and after treatment with bromergocryptine. Galactorrhea and amenorrhea were noted after pregnancy (6 patients), after oral contraceptive therapy (5 patients), and in association with pituitary adenoma (4 patients). Before treatment prolactin values were elevated ranging from 27 to 125 ng/ml, while luteinizing hormone and progesterone levels failed to show ovulatory peaks or luteal phase progression. Eleven patients had luteinizing hormone-releasing hormone tests before therapy. Response was normal in 8, subnormal in 2 pituitary adenoma, and supranormal in 1 patient with premature ovarian failure. Treatment with bromergocryptine was associated with a lowering of serum prolactin, cessation of lactation in all, and return of ovulatory menses in 14 of 15 patients. All relapsed when therapy was discontinued. Four patients became pregnant while on therapy. Long-term bromergocryptine therapy is effective for all forms of galactorrhea-amenorrhea syndromes studied.

Adenoma↗