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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test whether sustained midfollicular estrogen concentrations sensitize the pituitary response to GnRH in the continued presence of a GnRH stimulus, six female monkeys with regular menstrual cycles were administered hourly pulses of GnRH in the presence or absence of an sc estrone implant. Three were studied in a sequence of 2- to 8-week blocks of 1) control, 2) hourly pulses of exogenous GnRH (6 micrograms/1 min), 3) hourly GnRH pulses plus an estrone (E1) implant, and 4) the E1 alone. In the other three animals the sequence was 1) control, 2) E1, 3) E1 implant plus hourly GnRH pulses, and 4) GnRH pulses only. E1 increased mean estradiol concentrations from 55 pg/ml to 100 pg/ml and the corresponding E1 concentrations from 95 pg/ml to 160 pg/ml. LH concentrations, excluding midcycle surges, were 10.9 +/- 2.2 (SEM) ng/ml, 12.6 +/- 1.5 ng/ml, 11.7 +/- 1.5 ng/ml, and undetectable (less than 6 ng/ml) for the control, GnRH, GnRH plus E1, and E1-treatment periods, respectively. Of note was the suppression of LH concentrations to undetectable levels by midfollicular concentrations of estrogen during the E1-alone treatment period, and the return of LH concentrations to normal follicular phase levels by the application of exogenous GnRH support. This observation suggested that an estrogen negative feedback signal can suppress endogenous GnRH. To further examine this hypothesis we applied the same protocol to two hypogonadal female monkeys. E1 capsule placement increased the mean estradiol concentration from 22 to 61 pg/ml and suppressed LH and FSH to undetectable levels. When hourly pulses of GnRH (6 micrograms/1 min) were supplied, mean LH and FSH increased to 29.8 and 14.9 ng/ml, respectively. These studies demonstrate that elevation of estrogen concentrations to midfollicular levels does not sensitize the pituitary to GnRH stimulation, and pituitary sensitization is therefore unlikely to be important as a cause of elevated LH secretion in anovulatory states, such as the polycystic ovaries syndrome. In the hypogonadal monkeys, a 5-fold decrease in gonadotropin concentrations occurred in spite of full exogenons GnRH support, consistent with a hypophyseal site of estrogen negative feedback action. However, the GnRH clamp did prevent the complete suppression of LH and FSH noted when only estrogen was applied, consistent with an additional negative feedback effect on the hypothalamus. Although this same phenomenon is observed in the eugonadal monkeys, it appears unlikely that a hypothalamic site of estrogen inhibition plays a significant role during the menstrual cycle, otherwise the progressive rise in follicular phase estrogen concentrations would, by arresting GnRH secretion, abort folliculogenesis.
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PMID:Chronic hyperestrogenemia: lack of positive feedback action on gonadotropin-releasing hormone-induced luteinizing hormone release and dual site of negative feedback action. 153 75

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

The serum levels of bioactive luteinizing hormone (LH), immunoreactive LH, follicle-stimulating hormone (FSH), and testosterone were determined in eleven anovulatory women with polycystic ovary syndrome (PCOS) before and after laparoscopic ovarian cautery. Before treatment, the mean +/- SEM levels of bioactive and immunoreactive LH and testosterone were 53.1 +/- 7.9 mIU/ml, 35.2 +/- 3.9 mIU/ml, and 1.14 +/- 0.13 ng/ml, respectively, which were significantly higher than those of five control women (19.2 +/- 1.6 mIU/ml, 21.4 +/- 1.2 mIU/ml, 0.28 +/- 0.03 ng/ml). After treatment, the mean levels of these hormones decreased significantly, ten women ovulated spontaneously and four conceived. The present results suggests that decreases in the levels of these hormones by laparoscopic ovarian cautery in women with PCOS may result in both restoration of the ovulatory cycle and the achievement of pregnancy.
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PMID:Electrocautery in polycystic ovary syndrome. 212 80

Twenty-one nulliparous oligomenorrheic women with polycystic ovaries, complaining of infertility (mean duration 6 years) refractory to medical treatment, underwent laparoscopic ovarian diathermy. Eleven had adhesions and/or endometriosis. Regular ovulatory cycles ensued in 17 women (81%). In 9 responders there was a transient rise in mean follicle-stimulating hormone from 5.0 +/- 0.4 (standard error of the mean [SEM]) to 6.7 +/- 0.5 mIU/mL on postoperative day 1 and a fall in testosterone from 2.6 +/- 0.2 to 1.9 +/- 0.2 nmol/L by day 8. Luteinizing hormone fell from 19 +/- 1.2 to 10.4 +/- 1.2 mIU/mL by the follicular phase of the next cycle. Eleven women have conceived 13 pregnancies; 3 miscarried, 7 were delivered at term and 3 are ongoing. Ovarian diathermy is a useful option in women with polycystic ovaries complaining of refractory anovulatory infertility.
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PMID:Laparoscopic ovarian diathermy in the management of anovulatory infertility in women with polycystic ovaries: endocrine changes and clinical outcome. 213 36

We have investigated the hypothesis that hyperinsulinemia may cause the polycystic ovary syndrome (PCO) by directly stimulating gonadal steroidogenesis and/or gonadotropin secretion. 10 insulin-resistant women with PCO and 5 age- and weight-matched ovulatory normal women had pulsatile gonadotropin release, gonadotrope sensitivity to gonadotropin-releasing hormone, and sex hormone levels studied on two consecutive study days, basally and during the infusion of insulin (mean +/- SEM steady state insulin levels, 1,254 +/- 63 microU/ml PCO vs. 907 +/- 92 microU/ml normal, P less than or equal to 0.01). Insulin acutely increased mean delta (6 h minus prestudy) levels of androstenedione (A) (P less than or equal to 0.001) and estradiol (E2) (P less than or equal to 0.05) and decreased mean plasma pool (0-6 h) levels of testosterone (T) (P less than 0.05), nonsex hormone binding globulin-bound T (P less than 0.05), and dihydrotestosterone (P less than or equal to 0.01) in the PCO women. Insulin also decreased mean plasma 6 h A to estrone (E1) ratios and increased 6 h E1 levels (both P less than or equal to 0.05) in the PCO women. There were significant sequence effects (insulin + day) in the PCO women on T/E2 ratios, indicating a carryover action of insulin. Insulin had no effects on gonadotropin release in the PCO women. In the normal women, the only significant change was an insulin or study day effect that increased mean 6 h E2 levels (P less than or equal to 0.01). There were significant spontaneous decreases in mean luteinizing hormone (p less than 0.05) and follicle-stimulating hormone levels (p less than or equal to 0.01) in the PCO but not the normal women on the second day of study. This study indicates that insulin can directly alter peripheral sex hormone levels independent of changes in gonadotropin release in insulin-resistent PCO women. Insulin decreased the levels of potent androgens in PCO women and did not increase androgen levels in normal women, arguing against a simple, direct causal relationship between hyperinsulinemia and hyperandrogenism in PCO.
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PMID:Insulin administration alters gonadal steroid metabolism independent of changes in gonadotropin secretion in insulin-resistant women with the polycystic ovary syndrome. 264 19

Arginine vasopressin responses to osmotic (0.1 ml.kg-1.min-1 NaCl), orthostatic (standing upright and maintenance of orthostatic position for 20 min), and hypoglycemic (0.15 IU/kg insulin) stimuli were evaluated in women with polycystic ovaries and in normal subjects. Blood dehydroepiandrosterone, dehydroepiandrosterone sulphate, androstenedione, testosterone, cortisol, and endogenous insulin levels were significantly higher in women with polycystic ovaries than in controls, whereas estrone, estradiol-17 beta, progesterone and 17OH-progesterone concentrations were normal in all subjects. Arginine vasopressin basal levels (mean +/- SEM of 3 test days; women with polycystic ovaries: 2.8 +/- 0.2 pmol/l; controls: 2.7 +/- 0.2 pmol/l) and secretory responses to orthostatic (mean peaks 100% higher than baseline values) and to hypertonic (130% increments) stimuli were similar in the two groups. Arginine vasopressin responses to hypoglycemia were lower in women with polycystic ovaries (50% increment) than in controls (150% increment), although comparable blood glucose decrements and GH or cortisol increments were found in the two groups. Arginine vasopressin peak responses to hypoglycemia were negatively correlated to testosterone, androstenedione, and endogenous insulin levels, but did not correlate with basal and hypoglycemia-induced peak cortisol concentrations or with circulating levels of other steroids. These data indicate a hypothalamic posterior pituitary disorder affecting arginine vasopressin response to insulin-induced hypoglycemia in women with polycystic ovaries syndrome associated with elevated blood androgen and insulin concentrations.
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PMID:Arginine vasopressin secretion in non-obese women with polycystic ovary syndrome. 269 74

Twenty-nine patients with polycystic ovary syndrome (PCOS) and 30 normal women had lipoprotein lipid and androgen profiles compared after a 12-h fast. Both PCOS and normal women were evaluated in the proliferative phase of the cycle. PCOS patients had higher serum LH to FSH ratios [2.0 +/- 1.3 (+/- SEM) vs. 0.6 +/- 0.1), higher testosterone (T; 66 +/- 5 vs. 33 +/- 2 ng/ml), higher free T (1.1 +/- 1 vs. 0.4 +/- 0.02 ng/dl), and higher dehydroepiandrosterone sulfate (291 +/- 28 vs. 140 +/- 12 micrograms/dl) levels, and lower T-estrogen-binding globulin-binding capacity (1.5 +/- 0.2 vs. 2.2 +/- 0.1 micrograms/dl) than normal women (all P less than 0.05). The PCOS patients had higher mean serum triglycerides [122 +/- 11 (+/- SEM) 63 +/- 3 mg/dl] and very low density lipoprotein cholesterol levels (24 +/- 2 vs. 13 +/- 1 mg/dl), but lower high density lipoprotein cholesterol levels (43 +/- 2 vs. 58 +/- 2 mg/dl; P less than 0.05). While PCOS patients were heavier and more sedentary and their diets were higher in saturated fat and lower in fiber (P less than 0.01, respectively), the differences in lipoprotein lipid concentrations could not be attributed to body weight. T-estrogen-binding globulin-binding capacity correlated with high density lipoprotein cholesterol in PCOS patients (r = 0.42; P = 0.025) after adjusting for weight. We conclude that hyperandrogenemia in women may result in a male pattern of lipoprotein lipid concentrations. These findings suggest that PCOS patients may have increased atherogenic potential.
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PMID:Lipoprotein lipid concentrations and cardiovascular risk in women with polycystic ovary syndrome. 404 82

The objective of this study was to evaluate whether the degree of suppression of ovarian volume effected by a gonadotropin releasing hormone (GnRH) agonist in patients with polycystic ovary syndrome (PCOS) correlated with basal insulin secretion and insulin secretion provoked by a glucose challenge. Eighteen PCOS patients received the GnRH agonist D-tryptophan-6-LHRH (Decapeptyl, 3.75 mg monthly i.m.) for 6 months and had blood glucose and insulin measured during a 75 g oral glucose tolerance test (OGTT) prior to and at the end of therapy. According to ovarian volume suppression after GnRH agonist therapy, two groups were defined: in group A (n = 10; mean body mass index (BMI) +/- SEM, 25.6 +/- 1.6 kg/m2) ovarian volume regressed from 17.9 +/- 1.6 to 6.7 +/- 0.3 ml (full responders) and in group B (n = 8; mean BMI +/- SEM, 28.1 +/- 2.3 kg/m2) from 21.5 +/- 1.1 to 15.1 +/- 1.0 ml (partial responders). Results showed that GnRH agonist therapy did not affect significantly BMI or fasting levels and area under the curve (AUC) for glucose and insulin in the respective groups. Fasting insulin levels correlated positively with ovarian volume prior to (r = 0.56, p < 0.05) and after 6 months of GnRH agonist therapy (r = 0.80, p < 0.005). The suppressibility of ovarian volume with GnRH agonist therapy correlated negatively with the difference between maximal and basal levels (r = -0.68), the area under the curve (r = -0.62) and maximal levels (r = -0.72) for insulin during the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of insulin in ovarian size in patients with the polycystic ovary syndrome. 784 5

Adipose tissue was used to characterize the metabolic abnormality of insulin resistance in polycystic ovary syndrome (PCOS). Nine patients with PCOS were studied during a period of amenorrhea and confirmed to be chronically anovulatory by vaginal ultrasound and plasma progesterone measurements. These were compared with six age- and body mass index (BMI)-matched controls (BMI, 27.2 +/- 2.2 in PCOS and 24.7 +/- 2.3 in control subjects). Insulin receptor binding was measured and insulin action was assessed by measuring initial rates of 3-O-methylglucose uptake and by inhibition of lipolysis. The maximum specific insulin receptor binding was 0.62% +/- 0.12% and 1.78% +/- 0.18% per 10-cm2 cell surface (mean +/- SEM) in PCOS and control subjects, respectively (P < .001). Maximum rates of glucose transport were also impaired as compared with controls, with 3-O-methylglucose transport being 0.90 +/- 0.15 versus 1.57 +/- 0.28 pmol/10 cm2/5 s, respectively (P < .05). The concentration of insulin required for half-maximal stimulation of glucose uptake was 165 +/- 36 versus 32 +/- 10 pmol in PCOS and control subjects, respectively (P < .05). The maximum percentage lipolysis inhibition (mean +/- SEM) was 9.5% +/- 1.6% in PCOS and 28.3% +/- 7.2% in control patients, respectively (P < .01). These data demonstrate that there are both insulin binding and postreceptor defects in adipocytes from amenorrheic PCOS subjects. The degree of defect in adipocyte insulin action is greater than would have been anticipated from in vivo data.
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PMID:Severe impairment of insulin action in adipocytes from amenorrheic subjects with polycystic ovary syndrome. 799 Jul 8

To investigate a possible role of ultrasound-guided follicular aspiration in the induction of ovulation in patients with polycystic ovaries (PCO). Serum concentrations of immunoreactive LH (I-LH), bioactive LH (B-LH), FSH, androstenedione, testosterone (T), dehydroepiandrosterone sulfate, E1, E2, and progesterone before and after the follicular aspiration were examined. Follicular aspiration was carried out 7 days after hCG administration in twelve patients refractory to ovulation induction with clomiphene-hMG-hCG. Concentrations (mean +/- SEM) of I-LH, B-LH, and T on day 3 of the menstrual cycle after the aspiration were significantly lower than those before the aspiration (4.8 +/- 0.5 vs 12.6 +/- 1.0 mIU/mL, 18.1 +/- 2.1 vs 50.0 +/- 4.1 mIU/mL, 45.4 +/- 5.0 vs 60.8 +/- 7.1 ng/dl, respectively; p < 0.01). The pattern of LH secretion in response to GnRH challenge test was also normalized after the aspiration. A significant decline in serum levels of E2 and T (p < 0.001) was observed 2h after the aspiration. The ovulation rate was 83.3% (10/12), and one patient achieved pregnancy after the aspiration. The present study suggests that an acute decline in serum levels of ovarian steroids after the aspiration possibly acted on the hypothalamo-pituitary axis of the patients to normalize sensitivity, and the treatment could release the patients from an endocrinologically-mediated vicious cycle and result in the achievement of ovulation.
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PMID:[A possible role of ultrasound-guided follicular aspiration in induction of ovulation in patients with polycystic ovaries]. 818


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