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)

Plasma levels of gonadotropins, PRL, T4, and adrenal and gonadal steroids were measured in two groups of 7- to 9-yr-old and 10- to 11-yr-old obese prepubertal girls, and were compared to those found in groups of nonobese girls of the same age. The data found in normal weight subjects confirm the data reported in the literature, showing a significant rise between the 7- to 9- and 10- to 11-yr groups, of FSH, pregnenolone, dehydroepiandrosterone, testosterone, and estradiol plasma levels, while LH, PRL, T4, cortisol, progesterone, 17-hydroxyprogesterone (17P), and androstenedione remained constant. In the obese subjects, pregnenolone and dehydroepiandrosterone levels are notably higher than in the normal girls, in the same range as those found in adult women; furthermore, they show no rise between the two age groups. The obese prepubertal groups had significantly higher progesterone, androstenedione, and PRL levels in comparison with those observed in girls of normal weight, but 17-hydroxyprogesterone, cortisol, testosterone, LH, and T4 were similar in both groups. Estradiol levels were markedly depressed in the obese girls; FSH levels were higher in the younger girls than in normal subjects. These data indicate that in prepubertal obesity, maturation of adrenal gland function (chiefly the delta 5 pathway), is notably enhanced, whereas gonadal secretion of estradiol is impaired in the presence of high levels of FSH and PRL.
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PMID:Plasma levels of gonadotropins, prolactin, thyroxine, and adrenal and gonadal steroids in obese prepubertal girls. 16 19

Previous studies have shown that the sensitivity of tissues to insulin is diminished in states of glucocorticoid and GH excess and is increased when these hormones are deficient. To evaluate the role of the insulin receptor in these states, we have studied [125I]insulin binding to purified liver plasma membranes obtained from rats with a variety of perturbations of both glucocorticoids and GH. Glucocorticoid excess was produced in rats by administration of ACTH (40 U/day for 4 days) or dexamethasone (1 mg/day for 4 days). This resulted in an insulin-resistant state. Associated with this insulin resistance, there was a 50-60% decrease in insulin binding to its specific receptors in liver. Conversely, adrenalectomy, which produces an increase in insulin sensitivity, was associated with an increase in insulin binding to liver. Computer-assisted Scatchard analysis using a negative cooperative model for the inulin-receptor interaction indicated that, in contrast to our findings with obesity, the changes in insulin binding in these states were most likely due entirely to changes in receptor affinity, with no change in receptor concentration. GH administration also produced mild insulin resistance and a decrease in receptor concentration. This was associated with a reciprocal increase in receptor affinity and thus, no major alteration in insulin binding occurred at low physiological insulin concentrations. Hypophysectomized rats, on the other hand, showed an increase in receptor concentration and a decrease in affinity, and GH treatment only partially corrected these changes. Rats implanted with the MtT tumor (which secretes ACTH, GH, and PRL) have the combined effects of excess glucocorticoids and GH and are very insulin resistant. Liver membranes prepared from these rats showed a decrease in insulin binding and receptor affinity similar to that observed in other states of glucocorticoid excess. Further, adrenalectomy of the tumor-bearing rats resulted in an increase in insulin binding despite the persistence of the elevated levels of GH, ACTH, and PRL. These findings suggest that alterations in insulin receptor affinity and number may play a major role in the states of altered insulin sensitivity which accompany glucocorticoid excess and deficiency, and follow hypophysectomy. In contrast, the insulin resistance associated with GH excess is mediated at either a site on the receptor distal to the insulin-binding site (i.e. transduction) or at one or more of the intracellular reactions important in insulin action.
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PMID:Alterations in insulin binding induced by changes in vivo in the levels of glucocorticoids and growth hormone. 21 65

The role of the neurotransmitter serotonin (SER) in regulating the hypothalamic-pituitary function is not completely clarified, although considerable evidence suggests a dominant stimulatory control of ACTH and PRL and a dominant inhibition of TSH, with more variable effects on GH secretion. Furthermore, SER has been implicated in the regulation of appetite, given the anorectic activity of SERergic drugs in animals and humans and experimental evidence suggesting that animal obesity can be a function of SER depletion. In order to study the hypothesized impairment of the SERergic system in human obesity, PRL, GH, TSH and cortisol levels before and after oral administration of the SER precursor 5-hydroxytryptophan (OH-TRY) (500 mg), were determined in 10 obese (BMI 41.5 +/- 1.68 kg/m2) but otherwise healthy women (mean age 50.9 +/- 1.43 yr) and in control group of 7 normal-weight (BMI 20.9 +/- 0.66 kg/m2) women (mean age 49.8 +/- 1.18 yf) after oral administration of the SER precursor 5-hydroxytryptophan (OH-TRY) (500 mg). The results were matched against placebo. In contrast with placebo, OH-TRY administration provoked a PRL and cortisol increase in all the subjects: PRL levels increased in controls at 120 min (p < 0.05) and at 180 min (p < 0.01) and in obese women at 120 and 180 min (p < 0.01); cortisol levels increased in both groups at 90, 120, 180 min (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of 5-hydroxytryptophan on the secretion of PRL, GH, TSH and cortisol in obesity]. 129 71

To evaluate the hypothesis that endocrine profiles change with aging independently of specific disease states, we examined the age trends of 17 major sex hormones, metabolites, and related serum proteins in 2 large groups of adult males drawn from the Massachusetts Male Aging Study, a population-based cross-sectional survey of men aged 39-70 yr conducted in 1986-89. Group 1 consisted of 415 men who were free of obesity, alcoholism, all prescription medication, prostate problems, and chronic illness (cancer, coronary heart disease, hypertension, diabetes, and ulcer). Group 2 consisted of 1294 men who reported 1 or more of the above conditions. Each age trend was satisfactorily described by a constant percent change per yr between ages 39-70 yr. Free testosterone declined by 1.2%/yr, and albumin-bound testosterone by 1.0%/yr. Sex hormone-binding globulin (SHBG), the major serum carrier of testosterone, increased by 1.2%/yr, with the net effect that total serum testosterone declined more slowly (0.4%/yr) than the free or albumin-bound pools alone. Among the major androgens and metabolites, androstane-3 alpha,17 beta-diol (androstanediol; 0.8%/yr) and androstanediol glucuronide (0.6%/yr) declined less rapidly than free testosterone, while 5 alpha-dihydrotestosterone remained essentially constant between ages 39-70 yr. Androstenedione declined at 1.3%/yr, a rate comparable to that of free testosterone, while the adrenal androgen dehydroepiandrosterone (3.1%/yr) and its sulfate (2.2%/yr) declined 2-3 times more rapidly. The levels of testosterone, SHBG, and several androgen metabolites followed a parallel course in groups 1 and 2, remaining consistently 10-15% lower in group 2 across the age range of the study. Subgroup analyses suggested that obese subjects might be responsible for much of the group difference in androgen level. Serum concentrations of estrogens and cortisol did not change significantly with age or differ between groups. Of the pituitary gonadotropins, FSH increased at 1.9%/yr, LH increased at 1.3%/yr, and PRL declined at 0.4%/yr, with no significant difference between groups 1 and 2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Age, disease, and changing sex hormone levels in middle-aged men: results of the Massachusetts Male Aging Study. 171 16

The concentrations of glycosylated (G-PRL) and nonglycosylated (non-G-PRL) forms of PRL and GH were measured during pregnancy in pigs of lean and obese (high backfat thickness) lines. Pregnant sows of the two genetic lines were killed, in groups of five to eight, at 60, 75, 90, and 105 days of gestation, and their pituitary glands and plasma were analyzed for the two hormones by immunoblotting, lectin-binding, and RIA techniques. In both lean and obese pigs, pituitary concentrations of G-PRL and non-G-PRL increased with advance in pregnancy, but there were no significant changes in either form of pituitary GH. Plasma concentrations of radioimmunoassayable PRL also increased with advance in pregnancy, with no consistent changes in serum GH concentrations. The dominant PRL constituent in plasma during the second half of pregnancy was G-PRL, and its concentration either increased or remained constant with advance in pregnancy. In contrast, plasma non-G-PRL concentrations decreased with advance in pregnancy in both lines of pigs, resulting in a steady rise in the plasma G-PRL/PRL ratio toward term. Compared to lean pigs, obese pigs had less radioimmunoassayable PRL and GH in their plasma and less GH (glycosylated as well as nonglycosylated) in their pituitary glands, but obese pigs had more G-PRL in their pituitary glands than lean pigs, and their plasma G-PRL levels tended to be higher and non-G-PRL levels lower than those of lean pigs. Pituitary concentrations of non-G-PRL in the two lines of pigs were similar. Overall, the results show a preponderance of G-PRL over non-G-PRL in the plasma of pregnant sows, with a preferential secretion of the glycosylated form during the latter half of pregnancy. Furthermore, they indicate a prevalence of higher G-PRL/PRL ratios in the pituitary glands of obese than lean pigs. These findings raise the possibility of a functional role for the glycosylated variant of PRL in the initiation and/or maintenance of events associated with pregnancy and obesity in the pig.
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PMID:Changes in the glycosylated and nonglycosylated forms of prolactin and growth hormone in lean and obese pigs during pregnancy. 236 78

To examine hormonal status in obese, gynecologically normal women we studied 25 regularly menstruating, massively obese (mean weight, 120 kg) women participating in a weight reduction program and 25 age-matched normal weight (mean weight, 60 kg) women. Serum 17 beta-estradiol (E2), estrone (E1), androstenedione (A), dehydroepiandrosterone sulfate, testosterone, LH, FSH, PRL, and cortisol concentrations were measured during the follicular phase of the menstrual cycle. Waist to hip ratio and abdominal fat cell size were measured at the beginning of the study. The serum levels of E2 (P less than 0.04) as well as those of A, SHBG, and LH (P less than 0.002) were lower in the obese group. Consequently, the testosterone to SHBG ratio and the E1 to A ratio were higher and the LH to FSH ratio was lower in this group. Waist to hip ratio did not correlate with the levels of circulating hormones or SHBG, but an inverse correlation was found between abdominal fat cell size and A as well as the LH to FSH ratio in the nonhirsute women of the obese group. Subsequent to moderate weight reduction (13.2 kg), serum A and E1 levels (P less than 0.01) increased, and serum cortisol levels decreased (P less than 0.001). Thus, massive obesity is associated with abnormalities in hormonal balance in gynecologically symptomless women, there being an association between E1, E2, A, LH, cortisol, and relative weight and/or abdominal fat cell size.
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PMID:Sex steroid, gonadotropin, cortisol, and prolactin levels in healthy, massively obese women: correlation with abdominal fat cell size and effect of weight reduction. 309 52

The effect of TRH administration on TSH and PRL release was investigated in 11 obese women and 16 normal weight women. There were no differences in basal serum levels of estradiol, T3, T4, TSH, or PRL between the 2 groups. The increment of TSH levels in the obese group [mean maximum change (delta max), 19.3 +/- 3.0 (+/-SEM) mIU/liter] was significantly higher (P less than 0.025) than that in the control group (delta max, 11.3 +/- 1.3 mIU/liter), whereas PRL levels rose significantly less (P less than 0.025) in these obese women than in the control group (delta max, 738 +/- 132 and 1311 +/- 133 mIU/liter, respectively). Since serotonin is known to stimulate PRL and inhibit TSH release, deficiency of serotonin has been hypothesized as the cause of this disparity between TSH and PRL levels in obesity.
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PMID:Disparity of thyrotropin (TSH) and prolactin responses to TSH-releasing hormone in obesity. 392 32

18 patients with "primary empty sella" were reviewed for this study. In 3 of them the sellar enlargement was discovered occasionally by performing skull radiographs for other reasons. The galattorrhea-dismenorrhea or amenorrhea syndrome and obesity were the most common clinical features. Endocrinological tests were normal in ten patients and abnormal in eight. Slight elevation of serum PRL was the most common record. 12 patients had enlarging of the sella turcica; in 4, only the floor was asymmetric and in 2 the sella was quite normal. In 5 patients C.T. without intra-thecal contrast was sufficient to discover the E.S. In 13 patients we performed C.T. cysternography by injecting in the lumbar subarachnoid space 8-10 ml of Iopamidolo 200. This is an excellent and safe technique to perform C.T. cysternography.
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PMID:[Primary empty sella. Clinico-radiologic considerations in 18 cases]. 403 90

To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Mean serum testosterone (T), androstenedione (A), dehydroepiandrosterone (D), D sulfate, and LH levels were significantly elevated in the PCO patients compared to those in control subjects. In PCO patients, the mean +/- SE basal insulin level (18.7 +/- 2.9 microU/ml) and the sum of the insulin levels in response to glucose (674 +/- 119 microU/ml) were significantly greater than those in the control group (11.0 +/- 0.8 microU/ml and 248 +/- 29 microU/ml, respectively). In all subjects, serum levels of T and A, but not D and D sulfate, were significantly correlated to basal insulin levels and insulin sums. Serum cortisol, GH, and PRL levels were similar in both groups. These results indicate that in PCO, a significant degree of insulin resistance exists, which clearly is not related to obesity. The positive correlation of serum T and A levels to circulating insulin levels in this study suggests that the insulin resistance in PCO may be, in part, a consequence of hyperandrogenism.
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PMID:Insulin resistance in nonobese patients with polycystic ovarian disease. 622 44

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


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