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)

Insulin-like growth factors IGF-I and IGF-II are bound to specific binding proteins in serum. The lower mol. wt binding protein (IGF-BP) has been detected in various tissues, including secretory endometrium and preovulatory follicles of the ovary. This group studied the circulating levels of IGF-BP in the serum of 23 patients with polycystic ovarian disease (PCOD) and found that one-third of them have a subnormal level. In comparison with PCOD patients with a normal level, those with a subnormal level had a higher degree of obesity and a tendency to be more hirsute. They also had a higher serum insulin concentration and testosterone/sex hormone-binding globulin (SHBG) ratio, but lower serum SHBG concentration than those with a normal IGF-BP level. PCOD is the second abnormal clinical condition, after insulinoma, in which subnormal serum IGF-BP concentrations have been reported. The significance of low serum IGF-BP levels to pathophysiology of PCOD remains to be elucidated by studies on local interaction between IGF-BP and insulin in the polycystic ovary.
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PMID:Low levels of low molecular weight insulin-like growth factor-binding protein in patients with polycystic ovarian disease. 246 7

Pulsatile GnRH administration for induction of ovulation is often ineffective in polycystic ovarian disease (PCOD) patients. To clarify and correct the endocrine mechanisms underlying this deranged response we gave pulsatile GnRH (5 micrograms, iv, every 60 min) to idiopathic hypogonadotropic hypogonadism (IHH) patients with primary amenorrhea for 19 cycles and to PCOD patients for 24 cycles before (pre-A) and for 25 cycles after (post-A) GnRH analog suppression. Compared to IHH, pre-A cycles were characterized by elevated LH, estradiol, and testosterone; reduced luteal phase progesterone; and low ovulatory (38%) and pregnancy rates (8%). Conversely, LH, estradiol, and follicular phase testosterone levels were lower in post-A than in pre-A cycles, while luteal phase progesterone was higher; the endocrine pattern of post-A cycles closely resembled the one of IHH cycles. The ovulatory and pregnancy rates of PCOD patients improved remarkably in post-A cycles (90% and 38%, respectively). Excessive body weight was associated with a lower incidence of ovulation in both pre-A (15%) and post-A cycles (75%). A worse endocrine pattern and a lower ovulatory rate (50%) were obtained when a second consecutive post-A cycle occurred without repeating GnRH analog suppression. No signs of even mild ovarian hyperstimulation and no multiple pregnancies were recorded in the post-A cycles. We conclude that in PCOD 1) deranged pituitary sensitivity, excessive ovarian androgen secretion, and obesity critically affect folliculogenesis and ovulation; 2) pituitary-gonadal suppression with a GnRH analog markedly improves the endocrine and clinical responses to pulsatile GnRH ovulation induction; 3) optimal results can be achieved only when each pulsatile GnRH cycle is preceded by GnRH analog suppression; and 4) pulsatile GnRH is highly effective and safe for ovulation induction, provided that PCOD subjects are pretreated with a GnRH analog.
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PMID:The abnormal response of polycystic ovarian disease patients to exogenous pulsatile gonadotropin-releasing hormone: characterization and management. 250 16

Several reports have shown elevated circulating beta-endorphin (beta-EP) levels in patients with polycystic ovarian disease (PCOD). However, it is not yet clear whether these high beta-EP levels are linked to the etiopathogenesis of PCOD or are secondary to the obesity. In the present study we measured beta-EP plasma concentrations in 19 PCOD patients, 10 with normal weight (Group A) and 9 with excessive weight (Group B), and in 18 normally ovulating women, 10 with normal weight (Group C) and 9 with excessive weight (Group D). beta-EP values were similar in the two groups of non-obese patients and controls. beta-EP concentrations were also similar in the two groups of obese patients and controls, and they were significantly higher (p less than 0.05) than in non-obese patients. Our data indicate that in PCOD, elevated beta-EP values are related to obesity, suggesting that they are not linked to the pathogenesis of PCOD.
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PMID:Plasma beta-endorphin levels in obese and non-obese patients with polycystic ovarian disease. 252 98

The relationship between sex hormones and the skin is increasingly considered to be very important. The skin has appropriately been called "A peripheral endocrine gland". In this review some aspects of the cutaneous metabolism of oestrogens, progestogens and particularly androgens are analyzed. Production of skin collagen is markedly enhanced by oestrogens. Progestogens with strong androgenic activity and especially androgens have a powerful stimulating action on all skin elements particularly the epidermis and the dermis the sebaceous glands and the hair. The skin manifestations of hyperandrogenism and disturbances of reproductive functions such as anovulation, oligoamenorrhoea and polycystic ovarian disease are usually the consequences of three main aetiopathogenic factors: the first is an abnormality of GnRH pulsatility related to central nervous system dysfunction and seemingly mediated by an increase in beta Endorphin, possibly related to some extent to changes in body weight and hyperinsulinism. The second aetiopathogenic approach is hyperaestronaemia secondary to obesity. Finally adrenal hyperandrogenism caused by different types of congenital adrenal hyperplasia or by increased sensitivity to ACTH may be implicated in these various clinical manifestations.
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PMID:[Sex hormones and the skin]. 269 19

To establish a rapid test for Cushing's syndrome we measured serum cortisol during and following iv dexamethasone infusion (5 micrograms.kg-1.h-1 for 5 h from 10.00 h) in simple obesity (N = 19) and in Cushing's syndrome (N = 12). We had first established that 5 micrograms.kg-1.h-1 was the lowest dose which consistently lowered serum cortisol in simple obesity. In obesity, serum cortisols ranged from undetectable (less than 30) to 48 nmol/l at 17.00, less than 30 to 37 at 19.00 and less than 30 to 38 at 08.00 h the following day. Serum cortisol at these three times did not show any overlap between simple obesity and Cushing's syndrome. Having established these findings we proceeded to study a group of patients with polycystic ovarian disease. These patients behaved differently. Their values at 17.00 and 19.00 h did not overlap those of Cushing's syndrome. However, at 08.00 h, 5 of the 7 had values within the range seen in Cushing's syndrome with a mean of 290 +/- 99 nmol/l. In conclusion, 17.00 and 19.00 h serum cortisol levels distinguish between Cushing's syndrome and both simple obesity and polycystic ovarian disease. However, in the latter, cortisol suppression is less prolonged than in simple obesity. This finding may be important for our understanding of the pathogenesis of the disease.
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PMID:A weight-related intravenous dexamethasone suppression test distinguishes obese controls from patients with Cushing's syndrome. 272 13

A study to determine serum lipids and lipoproteins in 54 women with polycystic ovarian disease (PCOD) who had varying body mass index (BMI) compared to the normal regular menstruating women was carried out. All patients had similar hormonal profiles of PCOD and differed from the control group. The significant observations were high level of triglyceride and low percentage of alpha lipoprotein in obese PCOD. The BMI was positively correlated with serum triglyceride level, beta and prebeta lipoproteins but inversely correlated with high density lipoprotein (HDL) cholesterol, the low density lipoprotein (LDL) cholesterol/HDL cholesterol ratio and alpha lipoprotein. No significant correlation between lipids, lipoproteins and testosterone levels was observed. It appeared that the alteration of serum lipids and lipoproteins in PCOD is due to the effect of obesity.
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PMID:Serum lipids and lipoproteins in women with polycystic ovarian disease with different body mass index. 290 6

The ovarian ultrasonic appearance in 20 patients with polycystic ovarian disease was studied and correlated to the clinical, hormonal, and laparoscopic findings. Ultrasound studies showed that both ovaries were enlarged in 15 patients (15.46 +/- 2.5 cm3). Maximum ovarian surface area was 9.75 +/- 3.38 cm2. Three ultrasonic patterns were detected: (1) isoechoic, with no discernible cysts (four patients); (2) hypoechoic, with multiple small cysts of less than 1 cm (11 patients); (3) hypoechoic, with single cyst of greater than 1 cm (five patients). Ultrasonic estimation of ovarian size was superior to clinical assessment and equal to that of laparoscopic examination. Subtle differences existed between the ultrasonic appearance of the ovaries in hyperprolactinemic subgroups of polycystic ovarian disease compared to normoprolactinemic ones. However, no significant relationship was found between the ovarian size and any of the hormones studied. Obesity, amenorrhea, hirsutism, hyperprolactinemia, and elevated testosterone and dehydroepiandrosterone sulfate levels were more common in the group with enlarged ovaries, whereas oligomenorrhea, elevated luteinizing hormone/follicle-stimulating hormone ratio, and elevated androstenedione and estrone levels occurred more frequently in the group with normal-sized ovaries. The value of ultrasound studies in the management of polycystic ovarian disease is emphasized.
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PMID:Correlation of the ultrasonic appearance of the ovaries in polycystic ovarian disease and the clinical, hormonal, and laparoscopic findings. 293 74

To determine the significant source(s) of estrogen production in women with polycystic ovarian disease (POD), 12 women underwent selective adrenal and ovarian vein catheterization, with simultaneous peripheral blood samplings for determination of cortisol, androstenedione (delta 4A), testosterone, estrone (E1), and estradiol (E2). Ovarian vein E2 gradients were observed in 11 of the 12 patients with a mean of 13.4, whereas adrenal blood samples did not demonstrate significant E2 gradients. Seven of 8 patients exhibited ovarian secretion of E1, with a mean gradient of 13.6 times that of peripheral blood, whereas 4 of the 8 adrenal samples showed E1 gradients. The mean value was 1.4 times peripheral levels. No significant correlations were found between peripheral E1 levels and body weight or degree of adiposity, nor was there a relationship between obesity and E1/delta 4A molar ratio in peripheral blood. The subjects with the highest ovarian delta 4A levels had a significant correlation between peripheral delta 4A and E1. Therefore, our data indicate a significant contribution of ovarian E1 secretion to the peripheral E1 pool in addition to the extraglandular conversion of delta 4A to E1. There was general lack of correlation between peripheral E1 concentrations and plasma E2, and these relationships versus body size suggest that the major source of E2 in women with POD was ovarian secretion.
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PMID:The source(s) of estrogen production in hirsute women with polycystic ovarian disease as determined by simultaneous adrenal and ovarian venous catheterization. 312 97

Polycystic ovarian disease has a variety of biochemical and clinical features with great individual variation. In our clinical experience, oligo-ovulation, manifested as oligomenorrhea or frank amenorrhea, associated with an acyclic estrogen milieu, is a consistent finding. This may be associated with hyperandrogenemia, hirsutism, inappropriate gonadotropin levels, hyperprolactinemia, obesity, insulin resistance, and ultrasound evidence of multicystic enlarged ovaries. A common presentation is infertility or irregular menstruation secondary to oligo-ovulation and hirsutism secondary to altered androgen metabolism. A challenge in diagnosis is to differentiate polycystic ovarian disease from latent cases of congenital adrenal hyperplasia. Although the precise mechanism in the pathogenesis of polycystic ovarian disease remains undefined, altered function of the hypothalamic-pituitary-ovarian and adrenal axes is both involved and integrated. Results from clinical trials of ovulation induction using different agents have implicated one site or another as the major progenitor of the "vicious cycle" but with no definitive pathway established. Restoring fertility to these patients can be challenging in that not all patients with polycystic ovarian disease respond to clomiphene or do so satisfactorily. The use of glucocorticoid suppression, pituitary suppression with GnRH analogues, or the use of FSH alone may be of benefit in clomiphene treatment failures.
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PMID:Polycystic ovarian disease. 332 31

Six nonobese women with polycystic ovarian disease (PCOD) showed significant hyperinsulinemia, compared with controls after oral glucose (P less than 0.05). As an indicator of insulin sensitivity, in vitro proliferation of erythrocyte progenitor cells of PCOD subjects exposed to physiologic concentrations of insulin was significantly blunted (P less than 0.001). Monocyte insulin receptor binding was not impaired in the PCOD subjects. Three of the PCOD patients were treated with a long-acting gonadotropin-releasing hormone agonist for 6 months, which resulted in marked suppression of ovarian androgen secretion but no demonstrable changes in in vivo or in vitro indicators of insulin resistance. Thus insulin resistance in PCOD subjects appears to be unrelated to ovarian hyperandrogenism (or acanthosis or obesity). Although certain tissues are insulin-resistant in PCOD patients, the ovary may remain sensitive and overproduce androgens in response to high circulating insulin levels.
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PMID:Persistence of insulin resistance in polycystic ovarian disease after inhibition of ovarian steroid secretion. 351 14


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