Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polycystic ovarian disease (PCO) is characterized by hyperandrogenism, ovulatory dysfunction, and altered gonadotropin secretion. Mean plasma FSH concentrations are low, while LH is elevated in a majority of patients. LH pulsatile secretion has been shown to occur at rapid follicular phase frequencies (approximately one pulse per h) in PCO, suggesting persistent rapid frequency GnRH secretion in this disorder. Anovulatory women with PCO were given estradiol (E2; Estraderm skin patches) and progesterone (P; vaginal suppositories) to produce midluteal concentrations for 21 days. The aim was to determine if E2 and P would slow LH (GnRH) pulse frequency and if this would result in augmented FSH secretion and follicular development after withdrawal of E2 and P. Plasma LH was measured every 10 min for 8 h before, during (days 10 and 20), and 7 days after withdrawal of E2 and P (day 28). On each of these study days FSH was measured hourly, and E2 and P were measured every 2 h. After sampling, GnRH (25 and 250 ng/kg, iv) was given to assess pituitary responsiveness. Follicular development was monitored by vaginal ultrasound through day 34 of the study. Basal LH frequency was 8.5 +/- 0.5 pulses/8 h (mean +/- SEM). During E2 and P, LH pulse frequency fell to 3.3 +/- 1.0 (10 days) and 2.3 +/- 0.8 (20 days), 39% and 27% of the basal value, respectively, and subsequently increased to 5.6 +/- 0.7 (66% of basal) 7 days after withdrawal of E2 and P. LH pulse amplitude (basal, 7.2 +/- 1.5 IU/L) was not reduced until day 20, but remained suppressed (3.9 +/- 1.1 IU/L) on day 28. As a result, mean LH (basal, 21.0 +/- 3.5 IU/L) fell progressively during E2 and P, to 3.8 +/- 1.2 IU/L on day 20, and remained low (39% of basal) 7 days after steroid withdrawal. Mean plasma FSH (basal, 7.1 +/- 0.9 IU/L) also fell during steroid administration, but in contrast to LH, had risen to 93% of the basal value by 7 days after E2 and P. LH release in response to exogenous GnRH revealed marked initial responses which did not decrease until day 20, but remained suppressed (8% of basal) after withdrawal of E2 and P. FSH responses were also suppressed on day 20, but had increased to 75% of the basal value by day 28. Initiation of follicular development occurred in all patients, and the lead follicle measured 12.3 +/- 0.8 mm 13 days post-E2 and P. Ovulation occurred in one patient.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reduction of gonadotropin-releasing hormone pulse frequency is associated with subsequent selective follicle-stimulating hormone secretion in women with polycystic ovarian disease. 190 45

Previous studies have shown that oral, but not transdermal, administration of estrogen stimulates GH secretion in postmenopausal women. Because GH impairs insulin action, the impact of estrogen replacement therapy on carbohydrate metabolism may be influenced by the route of administration. The aim of this study was to prospectively compare the effects of oral and transdermal estrogen replacement on glucose tolerance and insulin sensitivity in postmenopausal women. In an open label, randomized, cross-over study, nine postmenopausal women were randomized to transdermal estrogen patches (Estraderm-TTS 100) or oral conjugated estrogen (Premarin, 1.25 mg) daily for 12 weeks and then crossed over to receive the alternative treatment for a further 12 weeks. An oral glucose tolerance test and hyperinsulinemic euglycemic clamp (HEC) were performed before treatment and at the end of 10 weeks of treatment. Oral and transdermal estrogen both significantly reduced LH to the same degree. Mean GH did not significantly change with transdermal estrogen, but rose significantly during oral estrogen therapy. Peak and mean glucose and insulin levels during the oral glucose tolerance test were not altered by estrogen therapy and were not significantly different between treatments. Mean glucose and insulin levels were maintained at an identical level during the HEC performed at pretreatment and during estrogen therapy. The mean glucose infusion rate required to maintain euglycemia during the HEC (mean +/- SEM, pretreatment, 40.4 +/- 4.8 mumol/kg.min) was unaltered by oral (39.8 +/- 4.6 mumol/kg.min) or transdermal estrogen treatment (42.1 +/- 4.2 mumol/kg.min). However, during the transdermal estrogen phase (60 +/- 10 mumol/L), the mean nonesterified free fatty acid concentration was suppressed to a significantly lower level during the HEC than during the oral estrogen phase (120 +/- 20 mumol/L; P < 0.05). We conclude that compared to the oral route, transdermal estrogen therapy is associated with a slight, but significant, improvement of insulin action on lipid metabolism. However, in the short term, the route of estrogen replacement therapy does not have a major impact on glucose metabolism in postmenopausal women.
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PMID:A comparison of the effects of oral and transdermal estrogen replacement on insulin sensitivity in postmenopausal women. 777 23

The working hypothesis was that treatment of heifers with 17beta-oestradiol (E2) during specific periods of prepuberty would reduce the response of the hypothalamic-pituitary axis to E2 negative feedback and induce an earlier onset of puberty. The effects of chronic treatment with exogenous E2 administered at specific maturational phases on the age and weight at puberty were studied in 96 prepubertal Brahman (3/4-7/8 Bos indicus) heifers (187.0 +/- 3.3 days of age, mean +/- SEM), weighing 149.9 +/- 2.5 kg. Heifers were randomly assigned to one of six groups (n = 16 per group). Groups 2-6 received E2 implants (Compudose 200) for 90-day periods starting at 10, 13, 16, 19 and 22 months of age, while animals in group 1 remained untreated. Implants were placed subcutaneously at the base of the ear. Blood was collected for progesterone (P4) determination by radioimmunoassay (RIA) and the animals were weighed at monthly intervals from 6 to 15 months then weekly from 15 to 28 months of age. Puberty was defined by concentrations of P > 1 ng/ml in plasma and identification of a corpus luteum (CL) by transrectal ultrasonography (Aloka 210DX:7.5 MHZ probe). Treatment with exogenous E2 at any of the ages/treatment intervals evaluated in this study did not reduce age or weight at puberty (P > 0.7). The mean age and weight at puberty of control heifers was 735.3 +/- 19.7 days (range: 597-861) and 299.2 +/- 10.2 kg (range: 233-382), respectively, which is greater than the age and weight at puberty of 481 days and 246 kg, that was previously reported for B. indicus heifers [Post, T.B., Reich, M.M., 1980. Puberty in tropical breeds of heifers as monitored by plasmaprogesterone. Proceedings of the Australian Society of Animal Production 13, 61-62.]. The large variation in age and weight at puberty that was observed in the present study among heifers might indicate an individual animal effect to E2 treatment among some of the treated animals. The lengthy interval from birth to puberty observed in this study, as compared to other studies, reflects the effects of other factors such as genotype, environmental or nutritional influences on puberty.
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PMID:Treatment with 17beta-oestradiol does not influence age and weight at puberty in Bos indicus heifers. 1040 97