Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003128 (anovulation)
 1,718 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of alloxan-induced diabetes on ovulation and other ovarian responses were investigated in immature rats injected with PMS gonadotropin (PMSG, 15 IU/100 g) on day 30 of age. Rats were killed on day 32 (presumed proestrus) or on day 33, at which time the oviducts were examined for ova. Ovarian weight gain was similar in control and diabetic rats and Graafian follicles were present in both groups on day 32. None of the diabetic rats ovulated while 96% of the control rats ovulated. Anovulation in diabetic rats could not be attributed to a drug side-effect of alloxan or to a lack of ovarian responsiveness, as 90% of the animals ovulated after treatment with insulin or with hCG (5 IU). Measurements of serum estradiol and LH on the morning of presumed proestrus revealed that concentrations of these hormones were not different in control and diabetic rats. However, measurements of LH in blood samples taken in the afternoon from control rats showed an LH surge, whereas no LH surge was found in diabetic rats. Thus, anovulation in immature diabetic rats treated with PMSG is not caused by an attenuation of ovarian responsiveness or by decreased secretion of estradiol, but rather is due to the loss of the LH surge.
 ...
PMID:Etiology of anovulation in the immature alloxan-diabetic rat treated with pregnant mare's serum gonadotropin: absence of the preovulatory luteinizing hormone surge. 74 54

The protocol of investigation of seconday amenorrhea, based on a functional classification of the endocrine causes of anovulation is described. The investigation takes 6 weeks to complete. A blood sample is taken for the measurement of basal serum gonadotropins, prolactin, thyroxine, and free thyroxine index. X-rays are taken of the pituitary region. Serum estradiol level and the response to a combined injection of thyrotropin-releasing hormone and gonadotropin-releasing hormone can also be measured. Medroxyprogesterone acetate is given, 5 mg for 5 days, followed 1 week later by a 5-day course of clomiphene. The response to clomiphene is evaluated. The patient returns 6 weeks later and may undergo further investigations (pituitary tomography, intramuscular progesterone, and insulin hypoglycemia). Preliminary analysis of the results in 75 cases of amenorrhea who have all completed the above protocol reveals the commonest disorder to be a defect of negative feedback control of gonadotropin secretion (30%). 22% suffered from defects of cycle initiation. 22% had hyperprolactinemia. Ovarian failure accounted for 15% of the cases, but hypogonadotrophic hypogonadism was rare. A brief analysis of cost-effectiveness of this program is discussed.
 ...
PMID:Therapy-orientated diagnosis of secondary amenorrhoea. 77 6

The objective of this study was to elucidate the relationship and role of insulin-like growth factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), insulin and luteinizing hormone (LH) in the pathogenesis of polycystic ovary syndrome (PCOS). In a pilot study, serum concentrations of IGF-1 were determined in women with PCOS (n = 10), hypopituitarism (n = 12) and normal controls (n = 10). In the main study, serum concentrations of IGF-1, IGFBP-1, insulin and LH in women with anovulation associated (n = 23) and not associated (n = 47) with PCOS were determined. Serum concentrations of IGF-1 were not different in women with PCOS, anovulatory non-PCOS and healthy women but were low in those with hypopituitarism. Mean serum IGFBP-1 in PCOS (33.8 +/- 21.2 micrograms/l) was decreased compared with anovulatory non-PCOS (60.0 +/- 22 micrograms/l) (P = 0.0001), and correlated negatively with insulin concentrations (r = -0.67, P = 0.0006). Patients with PCOS could be separated into those with high LH and those with high insulin levels. It was concluded that women with PCOS have normal serum IGF-1 concentrations but IGFBP-1 levels, regulated by insulin, are low. Hyperinsulinaemia and raised LH are independently capable of stimulating ovarian androgen production. Growth factors may have an important role in the pathogenesis of PCOS.
 ...
PMID:The role of insulin-like growth factor-1 (IGF-1) and IGF binding protein-1 (IGFBP-1) in the pathogenesis of polycystic ovary syndrome. 128 82

Hyperinsulinemia type A, which is a very rare disease, is often manifested in menstrual disorders and/or anovulation. Recently, a 19-year-old woman diagnosed with hyperinsulinemia and acanthosis nigricans, visited our outpatient clinic complaining primarily of amenorrhea and hirsutism. Endocrinological studies revealed normal LH and FSH levels, low estradiol (42.3pg/ml) and high androgens (testosterone: Over 150ng/ml, delta androstenedione: 4.8ng/ml) in serum. Her fasting insulin level was excessively high (over 320 microU/ml). UST showed bilateral polycystic ovaries. These data support the hypothesis of a pathogenic mechanism of ovarian dysfunction in patients with hyperinsulinemia; that is, too much insulin stimulates ovaries directly, followed by the production of androgens and the formation of polycystic ovaries. Strict dietary management of this patient failed to cause spontaneous vaginal bleeding. Progesterone administration did not cause withdrawal vaginal bleeding. These findings suggest that the higher that insulin level is, the more difficult it is to induce ovulation.
 ...
PMID:[Primary amenorrhea and hirsutism associated with hyperinsulinemia type A]. 160 67

Many different disease processes can result in a phenotype of hirsutism, anovulation, and oligomenorrhea or amenorrhea. An important goal of reproductive endocrinologists is to identify specific genetic diseases that can produce the hyperandrogenic phenotype. Two genetic disorders that can result in the hyperandrogenic phenotype are 1) mutations in the 21-hydroxylase gene (adrenal hyperplasia), and 2) mutations in the insulin receptor gene (the syndrome of hyperandrogenism-insulin resistance and acanthosis nigricans). The identification of these two genetic causes of hyperandrogenism provides the opportunity to investigate new approaches to prenatal diagnosis and therapy, genetic analysis of pedigrees, and innovative forms of therapy.
 ...
PMID:Hyperandrogenism: new insights into diagnosis and therapy. 181

Our studies show that obese women with polycystic ovary syndrome are more likely to have hirsutism and menstrual disturbances than are lean women with PCOS. The most obvious biochemical differences between obese and lean women with PCOS is that SHBG concentrations are much lower in women with obesity. The SHBG levels are inversely related to insulin, and insulin has been shown to have a direct inhibitory action on SHBG secretion. Other factors, however, may contribute to the mechanism of the increased prevalence of hirsutism and anovulation in obese women with PCOS, such as a direct effect of insulin or increased activity of 5 alpha-reductase in peripheral tissues. Finally we have been able to show that weight reduction of more than 5% is associated with an improved biochemical profile and, importantly, with restoration of fertility.
 ...
PMID:Obesity and polycystic ovary syndrome. 205 54

Pregnancy and Cushing's syndrome are seldom found together (40 cases in the literature), since hyperadrenocorticism is often responsible for anovulation by gonadotropin suppression. We report the case of a 25-year old para II woman whose pregnancy was complicated by diabetes and arterial hypertension at 31 weeks and who received the conventional treatments (special diet, insulin therapy, pindolol). Caesarean section, motivated by premature rupture of the membranes, was performed at 37 weeks, delivering a healthy infant. The diagnosis of hypercortisolism with low ACTH level was made post partum. An adrenal tumour (the most frequent cause of Cushing's syndrome occurring during pregnancy) was removed after pre-operative treatment with ketoconazole, and endocrine functions returned to normal.
 ...
PMID:[Adrenal adenoma disclosing after delivery]. 209 25

The cult of a slim body without the slightest bit of adipose tissue and the food restriction or selection habits it creates are extremely common in our society. Their influence on menstrual cycle and female infertility is not negligible. A vegetarian low calorie diet may induce cycle disorders and a short luteal phase. Disturbances in the pulsatility of gonadotropic hormones are responsible for anovulation, and they occur when slimness with excessive reduction of the body fat mass is associated with psycho-socio-professional stress factors or with intensive sporting activities. The greater frequency of dysovulation in obese women, notably those who put on weight rapidly, is accompanied by numerous hormonal changes, including reduced sex hormone-binding globulin, increased ovarian and adrenal androgen production, increased peripheral aromatization of androgens to oestrogens, and altered gonadotropin pulsatile secretion. The hyperinsulinism consecutive to insulin resistance in obese subjects might act as co-factor of the luteinizing hormone and as such participate in abnormalities of follicular maturation by stimulating the insulin-like growth factor and the ovarian androgens. However, the relative importance of these various factors in the physiopathology of abnormal ovulation remains to be determined. Overweight reduces the effectiveness of clomiphene citrate, menopausal gonadotropins and gonadotropin-releasing hormone in stimulating the follicles. Weight loss reduces hormonal disturbances and facilitates follicular maturation and ovulation in spontaneous or induced cycles.
 ...
PMID:[Influence of abnormal weight and imbalanced diet on female fertility]. 214 38

We performed this study to clarify the independent effects of hyperandrogenaemia, hyperinsulinaemia, and obesity on lipid and lipoprotein levels in women with hyperandrogenaemia (HA) and anovulation which we designated as the polycystic ovary syndrome (PCO). We examined fasting lipid, lipoprotein, sex hormone and insulin levels in 38 women (21 obese (ob), 17 non-obese (nob] with HA and anovulation (PCO) and 38 normal ovulatory women (21 obese, 17 non-obese), matched for age and weight. The women with PCO had significantly increased androgen levels compared to the normal women. However, total oestradiol levels were similar in the PCO and normal women. Mean fasting insulin levels and 2-h glucose levels (both P less than 0.001) were significantly higher in ob PCO women. There were significant decreases (P less than or equal to 0.01) in high-density lipoprotein (HDL) levels in both the obese groups (ob PCO and ob normal) compared to the non-obese (nob PCO and nob normal) groups. Otherwise, mean lipid and lipoprotein levels did not differ in the ob or the nob PCO women compared to the control groups. The correlations between sex hormone, lipid and lipoprotein levels differed in the four groups of women. After statistical adjustment for potential hormonal interactions, nob PCO women had significant positive correlations between testosterone and LDL levels (R = 0.51, P less than 0.05) and insulin and TTG levels (R = 0.61, P less than 0.01). Ob normal women had a significant positive correlation between oestrone and TTG levels (R = 0.44, P less than or equal to 0.05). We conclude that (1) PCO women are in a low to risk for CVD primarily because of the increased prevalence of obesity rather than the reproductive hormone abnormalities associated with this disorder. However, by their lipid profiles, the PCO women were still in a low to intermediate risk group for CVD.
 ...
PMID:The independent effects of hyperandrogenaemia, hyperinsulinaemia, and obesity on lipid and lipoprotein profiles in women. 220 23

Polycystic ovary syndrome is a disorder of unknown cause characterized by anovulation, hyperandrogenism, and gonadotropin secretory abnormalities producing oligo-ovulation or anovulation. Hyperinsulinemia and insulin resistance are important features of this syndrome. Because other causes of androgen excess may produce similar clinical and biochemical findings, PCO remains a diagnosis of exclusion. Treatment is directed toward relieving symptoms of hyperandrogenemia in order to stimulate ovulation, correcting obesity, and inducing regular menses to reduce the risk of endometrial cancer.
 ...
PMID:Polycystic ovary syndrome. 226 12


1 2 3 4 5 6 7 8 9 10 Next >>