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

The responses of growth hormone, cortisol, and prolactin to symptomatic hypoglycaemia during an intravenous insulin tolerance test were measured in 20 massively obese subjects and six lean volunteers. In 11 subjects, who had been obese since early childhood, an impaired growth-hormone response and an absent prolactin response were found. In the nine other obese subjects, however, the growth-hormone and prolactin responses were not significantly impaired. Seven of these subjects had become obese either as a teenager or during adult life. These findings suggest the existence of two types of human obesity similar to those found in rodent models. In one the disorder of hypothalamic function may be due to a basic, possibly genetic abnormality, while in the other it is acquired.
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PMID:Evidence for existence of two types of massive obesity. 698 84

Obesity represents a metabolic abnormality which brings a disordered hormone response during functional pituitary tests. Twenty obese patients were investigated and growth hormone and prolactin response during the insulin tolerance test were determined and the result was compared to an adequate control group consisting of 10 healthy nonobese patients. Two types of prolactin response were obtained--one normal and one decreased, unlike the growth hormone response which was constantly decreased. The authors discuss the hypothesis according to which the defect of endocrine hypothalamus might be an etiological factor of obesity.
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PMID:Prolactin and growth hormone response in induced hypoglycaemia in obese patients. 702 62

The 24 hr mean plasma cortisol concentration was measured in 65 healthy women ranging from 21% below to 218% above desirable weight and in 47 healthy men ranging from 5% below to 330% above desirable weight. In the women, there was a clear-cut inverse linear correlation between the plasma cortisol concentration and the percent deviation from desirable weight (y = 7.5 -- 0.3 x; r = -0.49; p less than 0.001); the relation of free to total cortisol concentration was weight-invariant; the MCR of cortisol in the most obese women was much higher than that of nonobese women (340 +/- 76 versus 211 +/- 31 liters/gm urinary creatinine; p less than 0.01). In the men, the plasma cortisol level and MCR were weight-invariant. To account for the finding in women of a linear correlation of the decrement in plasma cortisol level with the percent deviation from desirable weight (which in turn is nearly perfectly correlated with the total body fat content), we postulate that a given weight of adipose tissue in women takes up a constant amount of cortisol; this in turn suggests that their adipose tissue contains a saturable binding system such as corticosteroid receptor. By the same logic, the weight-invariance of plasma cortisol and MCR in men suggests the absence of significant amounts of corticosteroid receptor in their adipose tissue. The finding that the increased cortisol MCR of obese women results in decreased plasma cortisol levels rather than an increase in cortisol production (the latter, corrected for muscle mass, is normal in obesity: Strain et al, Metabolism 29:980, 1980) suggests a defect in their cortisol ACTH feedback system. Such a defect, presumably hypothalamic, is not unexpected in the light of reports of defective hypothalamic control of prolactin and growth hormone secretion in obesity.
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PMID:Sex difference in the influence of obesity on the 24 hr mean plasma concentration of cortisol. 707 9

Hypocycloidal tomograms of the sella turcica and serum prolactin concentrations were obtained in 146 women with amenorrhea, galactorrhea, or both to diagnose prolactin-secreting pituitary adenomas. Findings suggesting an adenoma, ie, abnormal tomogram and elevated serum prolactin concentration, were found in 24.6% (16/65) of previously unscreened patients and 59.2% (48/81) of prescreened patients. The combination of an abnormal tomogram and elevated prolactin level was relatively specific for an adenoma, as 91% (42/46) of women with these findings who underwent surgery had histologically confirmed tumors. Tumors occurred in women from 15 to 45 years of age, with amenorrhea or galactorrhea ranging from less than six months to more than 20 years in duration. Some women in this series also had obesity, rapid weight loss, polycystic ovarian syndrome, amenorrhea following discontinuance of oral contraceptive use, or emotional stress.
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PMID:Prolactin-secreting pituitary adenomas. III. Frequency and diagnosis in amenorrhea-galactorrhea. 719 Oct 13

Obesity is a physiological state associated with alterations in hormone production and metabolism. These hormonal changes may bear on the increased risk for selected neoplastic disorders. Obesity is associated with increased estrone production in young and older women as well as in men. The source of this increased estrogen appears to be extragonadal metabolism of the prehormone androstenedione, which increases 3- to 4-fold in proportion to the obesity. In severe obesity, androstenedione production itself may be increased, providing extra prehormone for conversion to estrogens. In addition, obesity appears to shift peripheral metabolism of estradiol, resulting in decreased excretion of catechol estrogens which in turn may influence target organ stimulation. Testosterone production is unchanged in obesity; however, there are decreased levels of sex hormone-binding beta-globulin leading to increased clearance rates and spuriously low levels of circulating testosterone in both obese men and obese women. Alterations in sex hormone-binding beta-globulin may further lead to changes in "free" estradiol, which may play a role in target organ stimulation. Other changes noted in obesity include: (a) increased excretion of corticoid metabolites; (b) increased secretion of insulin but decreased insulin effectiveness; (c) blunted growth hormone responses to various challenges; and (d) possibly blunted prolactin responsiveness. There are no reasons at present to suspect that these changes influence cancer risk. With weight loss, sex hormone-binding beta-globulin changes are restored toward normal as are the elevated plasma estrogens and decreased testosterone levels. BEcause weight loss and dieting per se are associated with many physiological changes, hormonal measurements during these times are difficult to interpret. Few studies to date have been performed in formerly obese patients stabilized at their new weight.
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PMID:Obesity, hormones, and cancer. 726 Sep 28

It has been suggested that the well-documented relationship of dietary composition to the incidence of human breast cancer is mediated by the effects of dietary constituents on hormone levels. There is fairly good evidence for diet-hormone relationships in animals, but the evidence in humans is unconvincing. In this paper, we describe three of our findings relating nutrition to hormone levels: (a) that obesity causes retention of a tracer of estradiol in women but not in men, a finding we attribute to the presence of specific estrogen receptor in the adipose tissue of women but not men; (b) that obese men have elevated plasma estrone and estradiol levels but obese women do not, a finding we attribute to greater androstenedione-to-estrone conversion in the adipose tissue of men than in that of women; and (c) that cachectic girls with anorexia nervosa fail to have the normal nocturnal surge of prolactin secretion, a finding that we attribute to deficiency of tryptophan, which is an adequate stimulus for prolactin secretion. These findings give support to the concept that dietary factors affect hormone secretion and/or metabolism in humans.
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PMID:Influence of obesity and malnutrition on the metabolism of some cancer-related hormones. 726 Sep 51

Subnormal prolactin (PRL) and thyroid stimulating hormone (TSH) responses to thyrotropin releasing hormone (TRH) have been reported in massive obesity, while fasting and very-low-calorie diets have been shown to impair the reaction of PRL to TRH. The mechanism of these changes is poorly understood. We studied a group of moderately obese women on weight maintenance diets to determine whether PRL and TSH responses are reduced in moderate obesity, and repeated the TRH tests during treatment with a 320 kcal diet, with and without the addition of triiodothyronine (T3). Basal and maximal PRL levels after stimulation were not significantly different in the obese patients before dietary restriction from levels in non-obese controls. During the use of the diet the PRL response to TRH was significantly lower than the initial value (P less than 0.025) while basal PRL levels remained unchanged. The percentage reduction in PRL response showed a significant positive correlation with the percentage decrease in serum T3 (r = 0.80, P less than 0.05). Administration of 75 micrograms of T3 daily to the patients, however, was associated with a further significant decrease in the PRL response to TRH. Plasma oestradiol levels did not change with use of the diet. TSH response to TRH was normal in these patients and did not change with use of the diet alone. T3 treatment resulted in an almost complete suppression of the TSH response. In conclusion the reaction of prolactin to stimuli is normal in the moderately obese patient, but reduced during drastic caloric restriction. This decreased responsiveness is probably not due to changes in T3 or oestrogen levels.
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PMID:The effect of obesity and drastic caloric restriction on serum prolactin and thyroid stimulating hormone. 727 64

A genetic variant of the spontaneously hypertensive rat (SHR) has been produced which becomes markedly obese as well as hypertensive, i.e. Obese/SHR weigh 800 g as against 300 g for non-obese cohorts. Serum enzymes (CPK, SGOT, SGPT and LDH) are frequently abnormally elevated, concomitantly with a high incidence of myocardial necrosis. Obese/SHR are hyperlipidaemic with severe fatty infiltration of the liver; they are hyperglycaemic with enormous islets of Langerhans and extensive beta-cell degranulation; despite elevated blood urea nitrogen (BUN) levels, they manifest little or no renal damage. Measurement of corticosterone, deoxycorticosterone (DOC) and aldosterone in Obese/SHR demonstrate marked hyper-responsiveness to moderate stress. Circulating prolactin levels are lower in Obese and non-obese/SHR compared to SHR, but Obese/SHR manifest unusually high increases incirculating prolactin levels in response to stress. Obese/SHR are hyperinsulinaemic and have subnormal growth-hormone levels. Desite mild hypertension, hyperglycaemia and hyperlipidaemia, Obese/SHR show no evidence of atheromatous change but do develop early polyarteritis nodosa. It is believed that the genetically programmed hypertension and hyperglycaemia is mediated by increased DOC, aldosterone and corticosterone production respectively, and that the obesity, hypertension, and diabetes in Obese/SHR may be likened to human Cushing's disease.
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PMID:Pathophysiological differences between obese and non-obese spontaneously hypertensive rats. 742 76

Hyperphagia in rats fed a cafeteria diet might be related to the palatability of the diet or to diet-induced changes in central neurotransmitters regulating the feeding behavior. In this study the central serotonergic tonus in adult male Wistar rats was evaluated in vivo after 6 weeks of feeding a cafeteria diet by the prolactin response to the administration of 5-hydroxytryptophan (5HTP), the immediate serotonin precursor. Blood was taken just before, 30, 60 and 90 min after the ip injection of 50 mg/kg 5HTP for the determination of prolactin concentrations were comparable between cafeteria fed rats and control rats, fed normal laboratory chow (12.7 +/- 5.4 vs 7.7 +/- 4.5 ng/ml). The 5HTP-stimulated prolactin secretion in the cafeteria diet fed rats, determined by the peak value (95.8 +/- 17.2 vs 119.1 +/- 27.0 ng/ml) as well as by the integrated area under the curve (5478 +/- 774 vs 5916 +/- 2275 ng/ml. 90 min) was not significantly lower than in the control rats. In conclusion, our results did not show a significantly decreased 5HTP-induced prolactin release in cafeteria-fed rats, suggesting that a low hypothalamic serotonergic tonus is probably not involved in the overeating of this dietary-induced obesity model.
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PMID:5-Hydroxytryptophan-stimulated prolactin levels in cafeteria diet fed rats: an in vivo evaluation of the central serotonergic tonus. 769 11

The polycystic ovary (PCO) syndrome is frequently associated with obesity. That subset of women reportedly shows a much higher incidence of hirsutism and menstrual irregularities than do nonobese women with PCO syndrome. We evaluated the clinical features and hormonal profiles of 56 women with PCO syndrome and correlated them with the presence or absence of obesity. Thirty-eight (67.8%) of these women were obese (body mass index > or = 25 kg/m2). While presenting with the classic manifestations of PCO, they did not differ significantly from the manifestations of nonobese women with PCO syndrome. Although obese women with PCO had a lower incidence of oligomenorrhea as compared to nonobese women with PCO (57.9% vs. 83.3%, respectively) and amenorrhea was more frequent in the former group (42.1% vs. 16.6%, respectively), these findings are not statistically significant. The incidences of hirsutism and anovulatory infertility in the obese group as compared to the nonobese group were 81.6% vs. 77.8% and 28.9% vs. 27.8%, respectively (not statistically significantly different). The mean (+/- SE) serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), LH/FSH ratios, prolactin and testosterone were not statistically significantly different among the two groups. The present study found that obesity is common in PCO syndrome but that there are no significant differences in the clinical and hormonal characteristics of obese and nonobese women with it. Further studies are warranted to clarify the impact of obesity on clinical, metabolic and hormonal changes in PCO syndrome.
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PMID:Effect of obesity on the clinical and hormonal characteristics of the polycystic ovary syndrome. 783 28


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