Effects of Fasting on Luteinizing Hormone Dynamics in the Male Rat
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There is a monotypic change in basal serum gonadotropin levels following retinol treatment of chronically vitamin A-deficient (VAD) male rats. The present study was undertaken to investigate the hypothesis that the specific increase in serum follicle-stimulating hormone (FSH) represents a change in gonadotrope responsiveness to gonadotropin-releasing hormone (GnRH). To this end, a test dose of GnRH was given to VAD rats pre-, 5 days post-, and 10 days postreplacement of vitamin A (PVA). In VAD rats, basal serum FSH and luteinizing hormone (LH) levels were higher than those of controls. Increased LH/testosterone ratios, both in basal levels and in the secretory response to GnRH, suggested Leydig cell hyporesponsiveness in VAD animals. Both the FSH and LH responses to GnRH were maximal at 1 h, declining thereafter. Although the absolute increments in FSH and LH 1 h after GnRH in VAD rats were greater than in controls, the percent increase in FSH tended to be lower in VAD rats and to increase after vitamin A replacement. The specific enhancement of FSH release PVA became evident only when assessing total secretion of FSH and LH after GnRH. Luteinizing hormone response to GnRH increased PVA, but not significantly, while FSH secretion after GnRH increased both 5 and 10 days PVA, times during which basal FSH levels were also increasing. These changes in FSH secretion could not be attributed either to increases in endogenous GnRH or to changes in testosterone or estradiol levels. Basal serum androgen binding protein levels, elevated in VAD animals, did not respond to the acute increases in FSH after GnRH and remained high PVA, suggesting no acute change in Sertoli cell function. Thus, the PVA increase in FSH secretion unmasks a partial inhibition of the gonadotrope present in the retinol-deficient, retinoic acid-fed male rat.
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Advanced Glycation End Products (AGE) are proteins that can cause cell destruction by increasing oxidative stress and inflammation. This product resulted from a series of chemical reactions after an initial glycation reaction. A Leydig cell is one of the types of cells affected by AGE. This cell is located in the interstitial of the testes and stimulated by the luteinizing hormone. This study aimed to compare the luteinizing hormone receptor levels in Leydig cell culture of Sprague-Dawley rat induced by AGE only and the one that administered gamma-mangosteen. We conducted an experimental laboratory study on luteinizing hormone receptor levels in Leydig cell culture of Sprague-Dawley rats induced by advanced glycation end products 200 μg/mL and given gamma-mangostin 5 μM compared to the one that was not given gamma-mangostin. The highest mean of LHR level was in group 3 given gamma-mangostin 5 μM (8.06 pg/ cells/24h), and the lowest mean was in group 1 (control) (7.78 pg/ cells/24h). The LHR levels in the rats' Leydig cell culture given 5μM gamma-mangostin were higher than the other groups indicate the inhibition capacity on the oxidation process caused by AGE in aging rats Leydig cells culture.
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Radioimmunoassays for follicle stimulating hormone (FSH) and luteinizing hormone (LH) were used to determine the concentrations of these gonadotropins in sera from healthy men. No evidence of diurnal or other rhythmic variations in serum concentrations was found in samples obtained daily, 3 times a day, or hourly. Treatment of 3 subjects with 1.5 mg of ethinyl estradiol/day for 2–3 days resulted in a consistent fall in serum concentrations of both FSH and LH. Treatment of 3 subjects with 25 mg of testosterone propionate each day for 3 days resulted in a consistent fall in serum concentrations of LH. Treatment of 4 subjects with 200 mg of clomiphene citrate daily for 3 days resulted in a rise in serum concentrations of both FSH and LH.
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Previous studies have shown that reductions in Leydig cell testosterone production occur with aging in the Brown Norway rat. The recent observation that changes in luteinizing hormone (LH) pulse interval and amplitude also occur with aging suggests the possibility that age-related reduced Leydig cell steroidogenesis might be related to changes in LH. We reasoned that, if this is the case, exogenously administered LH should restore testosterone production by aged rat Leydig cells to the higher levels produced by Leydig cells of young rats. To test this hypothesis, young (4-month-old) and aged (21-month-old) rats received testosterone- and estradiol-containing Silastic implants designed to suppress LH and, thus, endogenous Leydig cell testosterone production. At the same time, the rats received miniosmotic pumps programmed to deliver pulsatile ovine LH at a predetermined daily dose. In some experiments, treatment effects were determined by measuring testosterone production by testes perfused in vitro with maximally stimulating ovine LH. In others, Leydig cells were isolated by centrifugal elutriation and Percoll density gradient centrifugation, and their in vitro ability to produce testosterone in response to maximally stimulating LH was determined. Testes or isolated Leydig cells from untreated young rats produced about twice as much testosterone as that produced by Leydig cells from aged rats. The administration of testosterone- and estradiol-filled implants for 5 days reduced testosterone production significantly at both ages. In young rats administered 24 microg LH/day for 5 days, along with the implants, testosterone production was maintained at the high level of the young controls. Comparable treatment of aged rats resulted in testosterone production only at the low level of the aged controls. Indeed, even with higher LH doses (36 microg/day), testosterone production by the aged rat Leydig cells did not rise above the aged-control level. The inability of exogenously administered LH to increase testosterone production by testes and Leydig cells of aged rats suggests that Leydig cell steroidogenic deficits in the aged Brown Norway rat are unlikely to be the result of age-related changes in LH.
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The gonadotropin extracts of 24-hr samples of urine of a postmenopausal woman were assayed by a general gonadotropin assay and by assays for follicle stimulating and luteinizing activity. By each of the 3 assay systems it was found that there was a 2-fold fluctuation in the amount of gonadotropin excreted from day to day.
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Human chorionic gonadotropin
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Serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were determined by radioimmunoassay in 6 subjects who had been exposed accidentally to 192Ir gamma rays. All subjects showed normal levels of LH and FSH shortly after the irradiation. From 100 to 150 days post-irradiation, however, serum FSH levels increased in subjects who received 12.2 rad or more, a finding in agreement with the decrease in sperm concentration below 10 millions/ml, while in the other 2 subjects who received 9.8 and 10.9 rad, it remained within normal range. The elevation in serum FSH levels in one of the severely exposed subjects (Y. S.) was noted as late as 413 days after the exposure, while the hormone levels in the all other cases declined toward normal level.
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