Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum binding capacity of sex-hormone binding globulin (SHBG-BC), steroid concentrations, and secretion patterns of LH and FSH were compared between groups of seven nonobese and seven obese patients with polycystic ovarian disease (PCOD). Obese patients with PCOD differed from those with normal weight in having very low SHBG-BC and elevated serum levels of free and albumin bound testosterone. Compared to healthy women in the follicular phase, both nonobese and obese patients with PCOD showed equally elevated serum levels of androstenedione, estrone, and albumin-bound and free estradiol. Pattern of gonadotropin secretion was studied from blood samples taken at 15 min intervals for 6 h. In 6 patients of both groups low pulses of FSH were found coincidently with pulses of LH. Serum level of LH showed a clear pulsatile pattern in all patients with PCOD, varying from 4.5 to 7.5 pulses per 6 h. The mean pulse rate in the groups of nonobese and obese patients with PCOD was similar, 5.9 pulses per 6 h. In the obese patients the mean LH levels were, however, less elevated and the pulse amplitudes were smaller than those in the nonobese patients. We suggest that this difference is due to high levels of biologically active testosterone in obese patients with PCOD.
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PMID:Obesity, serum steroid levels, and pulsatile gonadotropin secretion in polycystic ovarian disease. 622 11

The effect of a single dose of 150 mg depomedroxyprogesterone acetate (DMPA) on pituitary, ovarian, and endometrial function was assessed in relation to the peripheral levels of the compound in 8 women. The levels of DMPA, follitropin (FSH), lutropin (LH), prolactin, estradiol (E2), and progesterone (P) were measured 3 times/week during a pretreatment (control) cycle and then daily during postinjection weeks 14-17, 22-25, and 30-33. An endometrial biopsy specimen was obtained during postinjection weeks 17, 25, and 33. In 3 of 8 subjects the daily hormone assays carried out during postinjection weeks 30-33 indicated anovulatory periods; in these subjects, peripheral blood was drawn daily during postinjection weeks 46-49 and a 4th endometrial biopsy was taken during week 49. Plasma DMPA levels during the 14th postinjection week varied between 0.90 and 2.24 nmol/1, declined gradually, and became undetectable between weeks 17-24 (4 cases) or some time after week 33 (the other 4 cases). No correlation was found between the time when DMPA levels became undetectable and the obesity index.
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PMID:Return of ovulation following a single injection of depo-medroxyprogesterone acetate: a pharmacokinetic and pharmacodynamic study. 623 45

The Authors compared the mean LH, FSH, PRL, E1, E2, Testosterone, Androstenedione plasmatic levels in a group of post-menopausal women affected by endometrial carcinoma (EK), with those of a control group presenting clinical characteristics as close as possible to those of the pathologic group. The case series was significant. They found no significant difference between the two groups' hormonal levels. On the other hand, E1 levels were found to increase along-side with obesity. In patients affected by EK, E1 plasma levels significantly increased alongside with the post-menopausal age. Conversely, in the control group, this hormonal value significantly and progressively decreased from the menopause onwards. Furthermore, the Authors studied the effects of surgical intervention on the hormonal picture in EK bearers.
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PMID:Profiles and endocrine correlations in endometrial carcinoma. 640 36

To investigate the influence of obesity on hormonal parameters in 186 apparently healthy women and in 176 women suffering from severe obesity the serum concentrations of FSH, LH, estrone (E1), estradiol (E2), androstenedione (A) and testosterone (T) were determined radioimmunologically. The climacteric onset of increased FSH production is 4 yr earlier (P less than 0.001) in obese than in normal women. Parallel to the rise of FSH there is a significantly premature decrease of the E1 and E2 concentrations in obese women. The typical elevation of the LH was found similar and not significantly different in the two collectives. The mean A levels are significantly lower (P less than 0.01) in obese than in normal women in all age groups. The T concentrations do not depend on the age of the women during the investigated period (41 to 60 yr) and are significantly higher (P less than 0.001) in the obese than in the normal women. There is a significant (P less than 0.001) correlation between the concentrations of A and E1 both in the obese and the normal women. An increased conversion of androgens to estrogens by adipose tissue is not revealed by the peripheral serum concentrations. Our data clearly demonstrate that in obese women the onset of ovarian insufficiency is significantly earlier than in normal women.
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PMID:Influence of severe obesity on peripheral hormone concentrations in pre- and postmenopausal women. 640 84

10 examine the relationship between obesity and chronic anovulation, we compared basal serum LH, FSH, and PRL levels, determined at 20-min intervals, and basal C21 [progesterone, 17- hydroxyprogesterone , pregnenolone, 17-hydroxypregnenolone ( 17Pe ), and cortisol], C19 [testosterone (T), delta 4-androstenedione (A), and dehydroepiandrosterone] and C18 (estrone and estradiol) steroid hormone concentrations measured at 1- to 2-h intervals for a 24-h period in five normal weight cycling women (NC) and in two groups of weight-matched obese women. Five of the obese women were regularly cycling (OC), and six were amenorrheic (OA). Sex hormone-binding globulin (SHBG) and non-SHBG-bound T and estradiol concentrations were also measured in each woman. Compared to NC women, OC women had normal basal protein and steroid hormone concentrations, except for reduced 17Pe levels (P less than 0.05). Mean SHBG concentrations were reduced by approximately 30%, and non-SHBG-bound T was increased by 70%, although the differences were not significant. In addition, when six precursors of testosterone (pregnenolone, 17Pe , dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and A) were considered together as a group and the data analyzed by the kappa 2 test, a reduction in basal levels of these precursors was found in OC women relative to those in NC women (P less than 0.005). In OA women, mean concentrations of SHBG were markedly reduced and those of total T, A, estrone, and non-SHBG-bound T were significantly increased compared to those in both NC and OC women. Mean 24-h concentrations of LH tended to be greatest and FSH lowest in this group, but were not significantly different from those in the other groups. The mean LH pulse frequency was significantly greater in OA than in OC women (P less than 0.05). Mean 24-h PRL and cortisol levels were also reduced in OA women relative to those in NC women. These data suggest the possibility of a compensatory decline in total T production in OC women in an attempt to maintain normal hormonal homeostasis; as a consequence, ovulation continues in a cyclic fashion. In OA women, such compensatory mechanisms are no longer operative. Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women. In conclusion, our data imply that obesity is not a primary factor causing chronic anovulation. However, obesity may aggravate an already existing subtle defect in some women and result in amenorrhea.
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PMID:Endocrine comparison of obese menstruating and amenorrheic women. 642 58

The aim of the present study was to determine whether a group of patients selected on the basis of clinical features only is characterized by the typical hormonal findings as discussed in the literature concerning the PCO-syndrome. PCO patients had oligomenorrhea, secondary amenorrhea or otherwise evidence of chronic anovulation, as well as hirsutism and/or obesity. Control women had regular menstrual cycles and a normal body weight. Since androgen and estrogen production in women depends on the stage of follicular development, an effort was made to obtain endocrinological data under standardized conditions. Under well-defined circumstances the PCO group (n = 20) had higher LH levels and lower FSH levels as compared with the control group (n = 10). Consequently the LH/FSH ratio was significantly elevated in the PCO group. Serum estrone and estradiol levels were significantly elevated in the PCO group, as were the serum levels of androstenedione and testosterone. Despite these differences a marked degree of overlap existed in the PCO patients and the control women for gonadotropin, estrogen and androgen levels. It was concluded that although the presence of polycystic ovaries in the investigated PCO group of women was not confirmed by laparoscopy, laparotomy or histological examination of the ovaries, these women had basal endocrinological characteristics similar to those found in well-proven PCO patients reported in the literature.
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PMID:Hormonal characteristics of women with clinical features of the polycystic ovary syndrome. 643 Jul 30

The Laurence Moon Biedl Bardet syndrome is a polymorphous disease whose pathogenesis is still obscure. It is characterize by obesity, oligophrenia, polidactylia, retinitis pigmentosa, hipogonadism, but often there are various others symptoms. AA describe two cases. After a short explanation of de main features of this disease, they dwell upon the study of clinical objective symtomatology and upon instrumental and laboratory parameters regarding hormonal, metabolic and functional order of various organs and apparatuses. Both cases present all classic symptoms of this disease. In the first case we have noticed a deficit in LH and FSH, besides we have also noticed an asymmetry of the lateral ventricles of the brain prevalently on the right and a small increase in 17-KS and 17-OH-KS urinary. On the contrary in the second case we have noticed an EEG of epileptic type.
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PMID:[Lawrence Moon Biedl Bardet, a polymorphic syndrome]. 644 72

The aim of this research was to study both insulin secretion and insulin resistance index (IRI) in seventeen females, aged 16-30, affected by polycystic ovarian syndrome. The diagnosis was made using clinical, hormonal, radiological and echographic criteria. Eight healthy women, carefully matched with our patients for age and for statistical obesity incidence, were studied as controls. Both glycemic and insulinemic curves, areas, insulinemic/glycemic area ratio (IRI) were studied by tolbutamide test (1 g i.v.). Areas were assessed by planimeter, blood glucose by Trinder method, blood insulin by a RIA method, statistical study by t Student test and correlation coefficients. These latter were determined by comparing individual plasma testosterone, FSH, LH and LH/FSH ratio values together with urinary total 17-ketosteroid and delta HEA output values on the one hand and insulin areas and IRI values on the other. Increased glycemic areas, insulinemic peaks and areas, associated with markedly increased IRI values, were observed in the patients. A correlation exists between hyperinsulinism, insulin resistance on the one hand and increased urinary androgens output on the other. delta HEA resulted particularly increased over other androgenic fractions.
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PMID:[Hyperinsulinism and insulin resistance in the polycystic ovary syndrome as tested with tolbutamide]. 676 18

Twenty-three women considered to have polycystic ovarian disease (PCO) were studied in an effort to better understand the mechanism of inappropriate secretion (IGS) which is so characteristic of these women. Criteria for PCO included oligomenorrhea, infertility, an obesity index (ponderal index, PI) < 12, and an LH:FSH ratio > 3. The mean +/- SE weight and PI for this group were 175 +/- 7.5 lbs. and 11.2 +/- 0.2 respectively. Weight was not correlated with steroid levels in PCO or control women. The mean (+/- SE) of serum androgen concentrations (DHEA-S: 2.9 +/- 0.5 micrograms/ml; androstenedione: 2.6 +/- 0.3 ng/ml; and testosterone: 47 +/- 5 ng%) were all significantly higher than those in control women (p < .05). Total serum estradiol (E2) was comparable to those of controls in the follicular phase, while estrone (E1): E2 ratios averaged 2:1. Serum sex hormone binding globulin-binding capacity (SHBG-BC) averaged 56.8 +/- 4.2 nM which was significantly lower than that of controls (p < .05). The percent unbound E2 was significantly elevated in PCO (62% vs 37%). The mass of unbound E2 was also significantly higher in PCO women (40 +/- 3 pg/ml) than in controls (17 +/- 2 pg/ml) (p < .005). Serum LH:FSH ratios had a positive correlation with the relative and absolute concentration of unbound E2. In control women, unbound E2 correlated significantly with LH levels. This suggests that IGS characteristically found in PCO patients and exemplified by elevated LH;FSH ratios, is the result of the feedback response to elevated levels of unbound (i.e., biologically active) E2.
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PMID:Elevations in unbound serum estradiol as a possible mechanism for inappropriate gonadotropin secretion in women with PCO. 677 90

To examine the mechanism by which obesity influences ovulation, 55 patients with oligo- or anovulation were studied. Parameters measured in serum were sex steroid-binding globulin (SSBG), testosterone (T), PRL, LH, FSH, and estradiol (E2). The women were divided into 2 groups: an obese group (group 1), greater than 145% of ideal body weight, and a normal weight group, less than 120% ideal body weight. SSBG was measured by saturation analysis T, LH, FSH, PRL, and E2 were measured by RIA. SSBG group 1 levels were 7.14 ng dihydrotestosterone bound/ml compared to 14.7 ng dihydrotestosterone bound/ml in group 2 (P less than 0.05). There were no significant differences in FSH, T, or E2. The correlation of body weight vs. SSBG in all patients was r = -0.62. In these 2 groups, the SSBG was significantly lower in the obese patients compared to that in the normal weight patients, independent of T or E2 levels. SSBG correlated negatively with body weight, suggesting that obesity has an influence on SSBG levels independent of hormonal status. When SSBG is lowered, there may be an increase in free T which, by inhibiting follicular maturation, may begin the sequence of events seen in polycystic ovary syndrome.
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PMID:Obesity and its role in polycystic ovary syndrome. 678 98


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