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

To test whether short-term fasting has a different effect on hormone release from lactotrophs and thyrotrophs in normal-weight men compared with obese men, 10 mg metoclopramide (MET) was administered orally to seven normal and six obese men before and after a 56-hour fast. In the normal subjects, MET raised the serum prolactin (PRL) level before fasting from 5.1 +/- 1.3 to 58.6 +/- 9.5 micrograms/L in 60 minutes (P less than .02), but left the thyrotropin (TSH) level unaffected. An almost identical hormone response was seen after fasting. Obese men responded differently. Their lactotrophs were initially refractory to MET stimulation (PRL increase from 9.5 +/- 5.1 to 17.5 +/- 5.7 micrograms/L, NS), but became sensitive to such stimulation after fasting (PRL increase from 8.2 +/- 4.5 to 46.3 +/- 6.7 micrograms/L, P less than .01). The thyrotrophs were unaffected by MET before, as well as after, the fast. Although decreased PRL synthesis, reduced cell membrane permeability, and inadequate MET stimulation are plausible mechanisms by which the reduced PRL responsiveness to MET could be explained in the obese patients, neither is likely in view of the fact that the lactotrophs responded promptly to thyrotropin-releasing hormone (TRH), administered intravenously (IV) 60 minutes after MET, in the fed obese patients (PRL increase after TRH from 17.5 +/- 5.7 to a maximum of 48.0 +/- 8.7 micrograms/L, P less than .05). Furthermore, a 50% reduction of the MET dose (5 mg) resulted in a significant PRL response in non-obese healthy men (PRL increase from 3.1 +/- 1.1 to 40.3 +/- 0.9 micrograms/L, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased dopaminergic control of prolactin secretion in male obesity: normalization by fasting. 189 23

This retrospective review of pediatric patients with pituitary tumors causing onset of symptoms by 17 years of age was done to define their pathological distribution, clinical presentation, treatment, and prognosis. Eighteen patients were evaluated and treated from 1979 to 1989. Five had Cushing's disease and 13 had prolactin-secreting tumors. The mean age at the onset of symptoms was 14.7 years, with a range of 7 to 17 years. The mean follow-up period was 4.6 years, and the series consisted of 15 girls and 3 boys. Four of the 5 patients with tumors secreting adrenocorticotropic hormone were girls. The five patients exhibited obesity, hypertension, and growth retardation. The mean age of this group of patients at diagnosis was 12.2 years, and all had intrasellar lesions removed by the transsphenoidal approach. Adenoma was documented in 4 cases by histopathology. There was complete resolution of the endocrinological and clinical abnormalities in each case. The group of patients with prolactinomas comprised 11 girls and 2 boys, and their mean age at diagnosis was 15.7 years. The girls exhibited either primary or secondary amenorrhea. Seven had macroadenomas and 4 had microadenomas. Nine of the 11 girls underwent transsphenoidal resection, and surgery failed in 6, based on hormonal or radiological data. The two boys had suprasellar tumor extension and required multiple surgical procedures plus radiation therapy for control of the tumor mass.
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PMID:Pediatric pituitary tumors. 194 30

In this study we have examined the relationship between obesity and endocrine glands. We have underlined that obesity can be a symptom of some endocrine diseases and that, on the other side, only a few number of cases with excessive weight have a true endocrine pathogenesis. The endocrine implications of essential obesity, only detectable with appropriate dynamic tests, are sometimes expression of an altered peripheral metabolism. The more relevant hormonal data that we will examine in details are: increase of insulin plasma levels, altered hypothalamic neuroregulation with consequence on the gonadotropin secretion and values of prolactin, growth hormone and cortisol.
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PMID:[Obesity: relationships with the endocrine system]. 203 64

In 19 patients with endometrial adenocarcinoma and in 17 healthy women, of approximate age and body weight, concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), estradiol (E2), progesterone (PRG) and cortisol were determined by means of the RIA method. Gonadotropins show significantly lower values in the examined patients (FSH = 22.7 +/- 20.5; LH = 13.7 +/- 8.4) in relation to the control group (FSH = 41 +/- 28.3; LH = 23.5 +/- 13.9; P less than 0.001) and significantly elevated values of PRL (383.7 +/- 270) in relation to the control group (268.1 +/- 165.7; P less than 0.005). The correlation of the E2/PRG and Relative Body Mass (RBM) ratio in the examined patients, shows a significant positive correlation indicating an excess of E2, towards which PRG is not opposed to in obese persons. A significant correlation of PRL and E2 elevated values in the patients affected, in contrast to the control group, was also found. These findings confirm the assertion that subtile changes which exist in the hormone relations of affected persons, are linked to obesity.
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PMID:[Obesity as a risk factor in patients with endometrial adenocarcinoma]. 207 77

In order to demonstrate the suggested failure of the serotoninergic system in human obesity and to evaluate the role of central serotoninergic activity in prolactin (PRL) and thyroid stimulating hormone (TSH) release in this condition, 13 euthyroid obese and 9 healthy women of normal weight were studied. A TRH test (200 micrograms i.v.) was performed before and after administration of fenfluramine (FF) 60 mg b.d. for 14 days. In the controls, FF did not modify the expected significant increase in PRL induced by TRH. In obese patients, however, the PRL levels was significantly increased after TRH, but the increase was less than in the controls. After FF, the PRL response to TRH was larger than in the pretreatment phase, with values similar to those observed in normal subjects. In neither group FF did change the TSH-stimulating effect of TRH, but the hormonal response in obese patients was greater than in the controls. The restoration of the responsiveness of PRL to TRH after central serotoninergic stimulation confirms the hypothesis that a failure of the serotoninergic system may occur in human obesity. Since FF does not interfere with the secretory pattern of basal and stimulated TSH in normal or obese subjects, the serotoninergic system does not seem to play a major role in the control of TSH secretion.
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PMID:Effect of fenfluramine on prolactin and thyroid-stimulating-hormone response to thyrotropin-releasing-hormone in obese and normal women. 212 37

To evaluate whether the inhibitory control of TSH and the stimulatory control of prolactin (PRL) secretion exerted by endogenous serotonin was altered in obesity, 22 obese men and 10 normal controls were tested with TRH (200 micrograms IV bolus) in the presence (experimental test) and absence (control test) of the serotonergic agonist fenfluramine (60 mg PO 90 min before TRH). Control and experimental tests were also performed in seven male patients with subclinical hypothyroidism and were repeated in the same obese subjects after substantial weight loss. Basal TSH levels were similar in control and obese men. Normal TSH responses to TRH (peak less than or equal to 14 mU/L) were observed in all normal controls (mean peak +/- SE 9.8 +/- 0.6 mU/L). In contrast, obese men were divided into two groups: nine in whom the TRH-induced TSH rise was higher than normal (group I: mean peak = 16.5 +/- 0.5 mU/L) and 13 in whom it was normal (group II: mean peak = 10.6 +/- 0.7 mU/L). The hypothyroid men all had elevated basal and TRH-stimulated TSH levels. Basal PRL concentrations were similar in the normal controls and both groups of obese subjects. The PRL response to TRH was lower in both group I and group II obese men than in normal controls and was similar between group I and group II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serotonergic control of TSH and PRL secretion in obese men. 212 15

The purpose of this study was to evaluate prolactin secretion in obesity. Basal level of serum prolactin and prolactin response after thyrotropin releasing hormone (TRH) were investigated in 20 obese patients and 20 healthy subjects well matched for age and sex. Obese patients had higher basal levels of serum prolactin than those of healthy subjects. Conversely, no significant difference in serum prolactin concentration was found at any time during TRH stimulating test. However obese patients showed incremental areas of serum prolactin slightly, but not significantly, lower compared to healthy subjects, probably because their basal levels were higher. In conclusion, the present study confirms that prolactin secretion is altered in obese patients. The discrepancy between basal levels and prolactin response during TRH stimulating test seems to indicate a deficiency in the dopaminergic inhibitor system.
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PMID:[Changes in secretion of prolactin in obesity]. 212 7

RIA tests to determine the blood levels of gonadotropins, prolactin and different fractions of androgens have shown that the time course of the endogenous level of gonadotropins and androgens in boys aged 9 to 16 with Il-III degree of obesity without clinical signs of disturbed puberty is of the same type as that in healthy boys. However much lower concentrations of testosterone and FSH with a high level of LH and dehydroepiandrosterone were noted in the former. A single administration of chorionic gonadotropin has shown that in normal puberty first develops a mechanism of rapid excretion of testosterone into blood with its maximum concentration in 24-48 h, followed by the development of a mechanism of long-term activation of androgenesis at later stages of puberty. Obese boys with delayed puberty after the type of adiposogenital dystrophy or the syndrome of wrong puberty, demonstrate a more marked blood level of testosterone and FSH than in normal puberty. The clinical level of delayed puberty is determined by the peculiarities of the hypothalamohypophyseal system: the syndrome of wrong puberty is characterized by a sharp rise of adrenal androgenesis leading to premature pubarche, a decrease in the sensitivity of gonads to LH with a simultaneous rise of its blood concentration. Moderate activation of androgenesis in the adrenal glands was observed in false adiposogenital dystrophy, the prepubertal level of LH secretion being preserved.
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PMID:[The characteristics of the sexual development of boys suffering from obesity]. 214 42

The most common signs of androgen excess in women are acne, alopecia, and hirsutism. Less common manifestations include android obesity, virilization, and acanthosis nigricans. These changes appear to be the result of excessive androgen production or increased target organ sensitivity. To evaluate excessive androgen production, an androgen screening protocol is recommended that includes measurement of dehydroepiandrosterone sulfate, testosterone, androstenedione, prolactin, follicular stimulating hormone, and luteinizing hormone. When androgen excess is confirmed, dexamethasone suppression is recommended to determine the source of the androgen(s). Once excessive androgen production is confirmed, more specific therapies can be administered.
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PMID:Diagnostic approach to androgen disorders in women: acne, hirsutism, and alopecia. 214 37

Human obesity shows clustering within families. The hypothesis for the presence of a major gene or genes acting in human obesity is supported by recent evidence from studies of obesity in adoptees and their biological parents and siblings. The heterogeneity of obesity may be demonstrated by the shape of fat distribution and the prolactin response to insulin hypoglycaemia. Fat distribution has been shown to have a genetic background whereas a primary disorder of hypothalamic function is suspected in obese women who show an impaired prolactin response to insulin-induced hypoglycaemia. We have investigated the possible association between fat distribution and hypothalamic function in 23 extremely obese, nondiabetic premenopausal women who have been characterized using their absolute body weight, body mass index (BMI), fat distribution (expressed as waist to hip ratio), fasting insulin, basal prolactin and prolactin response to hypoglycaemia. Fasting insulin values showed a significant correlation (P less than 0.05, R = 0.604) with increasing waist to hip ratio (upper body segment obesity), whereas the graded prolactin response to hypoglycaemia of the obese women showed a negative association with increasing upper body segment obesity (P less than 0.05; R = -0.446). No relationship was observed between fasting insulin and the prolactin response to hypoglycaemia. We suggest that this previously unrecognized association of an impaired prolactin response to hypoglycaemia and upper body segment fatness may be useful for the investigation of the genetics of obesity.
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PMID:Impaired prolactin secretion and body fat distribution in obesity. 219 12


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