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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

17 obese women were examined, 8 of which were diabetic and 9 affected only by essential obesity. These patients, all of whom had become obese during adult life and 8 control subjects were tested for IRI, GH and PRL levels in basal conditions and after infusion of TRH. In the obese and diabetic women fasting GH values were normal while IRI levels were higher than those of the control subjects. In all cases neither IRI nor GH variations during TRH stimulation test. There was no difference in the plasma levels of PRL between the 3 groups when examined in basal conditions. After TRH the hormone increased considerably in all the subjects. In the obese and diabetic obese women the incremental area did not present different values from those observed in the control subjects. In conclusion in insulin-independent diabetes, as in essential obesity, the pharmacological stimulus did not show any evident alteration of the specific hypofisary receptorial system that regulates the secretion of PRL and GH.
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PMID:[Prolactin response to TRH in insulin-dependent diabetes mellitus]. 677 39

17 women affected by essential obesity were examined, 9 of whom had become obese as adults (group A) and 8 had been obese since childhood (group B). In group A, fasting and after TRH, the PRL presented higher plasmatic levels than those found in the controls. In group B the hormone showed basal values and global secretory areas higher than those observed in the controls and in group A, while incremental areas did not result different from those found in the other groups examined. In no case did IRI, GH and glycaemia undergo changes in relation to TRH. In conclusion we think that the behaviour of prolactin can be an important physiopathological characteristic, expression of the different neuroendocrine hypothalamic homeostasis existent in the heterogeneous obese population.
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PMID:[Prolactin secretion in patients with essential obesity]. 678 37

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

To investigate a possible hypothalamic alteration in obesity, we have studied the pattern of PRL secretion in response to insulin hypoglycemia, arginine infusion and TRH injection in 12 grossly obese patients and in 12 normal-weight controls. In the obese patients, PRL secretion was significantly lower than in normal subjects in response to insulin hypoglycemia and arginine infusion, while it was not significantly different from that in controls in response to TRH. The mean +/- SE values of the areas subtended by the PRL curves in the 3 above tests were 54.7 +/- 155.81 vs 3677.3 +/- 520.30 ng/2h, p less than 0,01, 210.3 +/- 148.93 vs 1034.8 +/- 203.15 ng/2h, p less than 0.05 and 1476.8 +/- 275.13 vs 2148.6 +/- 682.06 ng/2h, NS, respectively, in the obese and in controls. These results are compatible with the concept of impaired hypothalamic control of PRL secretion in obesity, although it is still unclear what role this may play in the pathogenesis of this disorder.
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PMID:Impaired prolactin secretion in obese patients. 679 62

We report the case of a 17-year-old girl presenting short stature (height 149 cm, below the 3rd percentile), obesity (weight 83.5 kg, body mass index 37 kg/m2) and secondary amenorrhea, in whom endocrinological evaluation disclosed an absolute lack of GH responsiveness to both suprapituitary challenges and repetitive growth hormone releasing hormone administration together with failure of plasma gonadotropins and PRL, low under basal conditions, to rise in response to GnRH and insulin-hypoglycemia, respectively. In contrast, basal and stimulated TSH and ACTH secretions were normal. Radiological examination of the skull revealed virtual absence of the pituitary fossa due to the lack of sellar cavum and dorsum, while magnetic resonance was unable to detect any pituitary tissue. A mucosal cleft of the nasopharynx, compatible with a pharyngeal hypophysis, was disclosed at endoscopy. This is an unusual case of developmental abnormality including lack of formation of the sella turcica and incomplete caudal migration of the embryonal anterior pituitary, resulting in ectopically located--likely pharyngeal--pituitary tissue. In view of the occurrence of spontaneous menarche and of a growth impairment less severe than one would expect considering the degree of GH deficiency, it is conceivable that the ectopic pituitary tissue has lost, in time, some of its secretory ability.
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PMID:Abnormal development of the sella turcica and lack of pituitary visualization in a patient with partial hypopituitarism. 759 30

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55

To evaluate whether the PRL, TSH and gonadotropin secretion is altered in conditions with elevated body mass index, 7 patients with central Cushing's disease before and after transsphenoidal surgery, 7 untreated patients with Cushing's syndrome caused by adrenal adenoma, 17 simplex obese (obese) women and 9 non-obese controls (all females, aged 18-45 years) were tested with TRH (200 micrograms i.v. bolus) and GnRH (100 micrograms i.v. bolus) and the hormone responses were measured. There were no differences in the basal pituitary hormone secretion among the groups. In obese subjects the PRL response was reduced as compared to untreated patients with corticotrop pituitary adenoma. No significant differences of TSH release could be observed among the groups, whereas serum total T4 levels were higher in obesity than in patients with hypercorticism either caused by pituitary or adrenal Cushing's syndrome. No differences were found in the LH response, but the stimulated FSH release was lower in obesity, in patients with central Cushing's disease after transsphenoidal surgery and in patients with primary Cushing's syndrome as compared to the normal controls.
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PMID:[Anterior pituitary responsiveness in central Cushing disease and in Cushing syndrome caused by adrenal cortex tumors, as well as in simple obesity]. 786 32

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in response to GHRH, studied in three different situations characterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's syndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a control group 18 normal subjects of similar age and sex were studied. GH and PRL was determined at intervals after GHRH (1 microgram/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamethasone. In contrast, GHRH-induced PRL secretion was not affected in these three clinical situations. In summary, in three situations characterized for an impairment of the somatotroph cell, due to a primary intrinsic defect or to a functional hypothalamic alteration, there is a persistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hyposomatotropism.
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PMID:Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism. 788 70

This prospective study defines the clinical and biochemical features of acromegaly in a large cohort of patients. There was no difference in sex distribution, and for men and women the mean ages at diagnosis (40 +/- 12 and 40 +/- 14 yr, respectively) were similar. Nearly three-quarters of patients were overweight and some 12% severely overweight; the frequency and severity of obesity also was not different between the sexes. Half of patients were hypertensive or were taking anti-hypertensive drugs. Neither GH nor insulin levels were significantly different between normotensive and hypertensive patients. Acral growth and facial coarsening, soft tissue swelling, and excessive perspiration were present in the majority (98%) of patients. Mean serum GH, Sm-C, and PRL levels did not differ between the sexes. Sm-C levels correlated with mean GH concentration (r = 0.31, p < 0.001), both variables inversely related to age. With each decade of life, mean GH and Sm-C levels declined by 7.6 +/- 0.2 ng/mL and 0.5 +/- 0.2 U/mL, respectively. Impaired glucose tolerance was diagnosed in 36% and frank diabetes mellitus in 30% of patients. Hyperprolactinemia was noted in 18% of patients. Galactorrhea was noted in 43 (9%) patients, most of whom were female; the mean GH levels of patients with galactorrhea (60.1 +/- 13 ng/mL) were higher than those of patients without (35.4 +/- 2.6 ng/mL, p = 0.02). Acromegaly appears to afflict men and women equally with a preponderance of presentation in the fourth decade of life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acromegaly. Clinical and biochemical features in 500 patients. 793 7


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