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

Clinical value of plasma TSH radioimmunoassay in various thyroid diseases (primary hypothyroidism, hyperthyroidism and simple goiter) is discussed. In particular, the results obtained of plasma TSH after TRH administration either in thyroid disease either in various disorders of endocrinologic interest (massive obesity, Laurence-Moon Biedl's syndrome, true precocious puberty, congenital adrenal hyperplasia, Klinfelter's and Turner's syndromes) are discussed.
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PMID:[Clinical use in the radioimmunologic determination of plasmatic TSH]. 122 42

Fenfluramine is an amphetamine derivative which is used as a weight-reducing agent in the treatment of obesity. It has been postulated that fenfluramine affects brain serotonin (5HT) neurons resulting in decreased food intake and altered autonomic outflow which, in turn, increases metabolism. CRF decreases food intake and, in addition, has been demonstrated to reduce body weight in genetically obese rats through selective activation of sympathetic and inhibition of parasympathetic outflows. Because 5HT is a potent CRF secretagogue, we tested the hypothesis that the weight-reducing effects of fenfluramine administration may be mediated, in part, through altered CRF secretion. Chronic fenfluramine treatment (1-24 mg/kg sc, twice daily, 4 days) resulted in a dose-dependent decrease in hypothalamic CRF concentration at 30 min after the final drug injection and was accompanied by a significant reciprocal increase in plasma corticosterone concentration. These data suggest that the decrease in hypothalamic CRF was a consequence of increased CRF secretion. These changes in hypothalamic CRF and plasma corticosterone correlated with brain fenfluramine levels. In contrast, high dose fenfluramine treatment significantly increased hippocampus, midbrain, and spinal cord CRF concentrations whereas levels in cerebral cortex, caudate putamen, thalamus, pons/medulla, and cerebellum were unaffected. There was no effect of this fenfluramine treatment protocol on regional brain TRH or neurotensin concentrations. In keeping with the well known development of tolerance to the weight-reducing effects of fenfluramine, chronic fenfluramine treatment resulted in lesser increases in corticosterone secretion than after acute treatment. Whereas weight loss observed after chronic fenfluramine treatment was associated with stimulation of hypothalamic-pituitary-adrenocortical hormone secretion, the weight-recovery phase after cessation of drug treatment was associated with decreased levels of plasma corticosterone. These data, demonstrating fenfluramine-induced alterations in brain CRF and plasma corticosterone, suggest that CRF may represent an important endogenous transmitter which mediates the weight-reducing effects of the drug.
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PMID:Role for brain corticotropin-releasing factor in the weight-reducing effects of chronic fenfluramine treatment in rats. 164 65

The Authors examine serum levels of HPRL in basal conditions and after TRH and sulpiride test in 15 patients with endometrial lesions (hyperplasia) and in 15 patients with endometrial adenocarcinoma included in a age range between 44 and 62 years, in which 7 patients present obesity, 10 patients present hypertension and 2 patients are hyperglycemic. The same examination is carried out in a control group of 30 healthy patients. Then the 15 patients with adenocarcinoma and 3 patients with adenomatosa hyperplasia are subjected to surgery and they estimate HPRL levels in endometrium. The results prove that there is no correlation between HPRL plasma levels and endometrium lesions and between endometrium HPRL. The Authors conclude that HPRL does not play a significant role in the pathogenesis of endometrial lesions; use of HPRL plasma levels as a marker of endometrial lesions is not possible.
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PMID:[The role of prolactin in endometrial lesions]. 178 4

Circulating TRH-immunoreactive levels, the thyrotropin response to a TRH intravenous stimulation (200 micrograms) and thyroid hormone concentrations have been determined in 43 overweight subjects (body mass index 45 +/- 12 kg/m2, mean +/- s.d.) and 46 (body mass index 22 +/- 2 kg/m2) normal weight controls. The TRH levels measured by a recently developed, highly specific radioimmunoassay were similar among both groups (44 +/- 16 vs 40 +/- 12 fmol/ml, n.s.). The pattern of response of TSH to TRH was normal in the obese and no significant difference was observed between the peak TSH values of the obese and the normal group (8.3 +/- 2.8 vs 8.7 +/- 2.2 microU/ml, n.s.). No correlations were found between the degree of obesity and the concentrations of TRH, TSH and peripheral thyroid hormone levels. Three obese patients showed a delta-TSH of 18, 19 and 21 microU/ml at normal thyroid hormone concentrations as sign of latent hypothyroidism. These data indicate that in obesity: (a) the TSH response to i.v. TRH is not impaired, (b) circulating TRH-IR levels are not significantly changed and (c) the incidence of overt hypothyroidism is not increased.
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PMID:Thyrotropin releasing hormone (TRH) immunoreactivity and thyroid function in obesity. 190 Dec 99

The Laurence-Moon-Biedl syndrome is characterized by retinitis pigmentosa, obesity, psychic disturbances, polydactily and hypogonadism. Renal involvement is also a frequent finding and renal failure may be fatal for the patient. On the basis of the consanguinity and the familiarity of this syndrome. R.C., a 47 years old male, with cardiovascular failure and marked psychic sleepiness has been studied. The patient showed the full picture of this syndrome. The thyroid function has been studied and, TT4, TBG, rT3, TSH, TRH stimulation test, antimicrosomial antitireoglobulin antibodies were found within normal limit. On the other hand TT3, FT3, FT4 and 131-I thyroid captation showed a clear hypothyroidism picture. In this connection, on L-T4 administration, infect there was a complete recovery of the symptoms. This picture may confirm the hypothesis of a hypothalamic disfunction in the Laurence-Moon-Biedl syndrome.
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PMID:[Laurence-Moon-Biedl syndrome associated with tertiary hypothyroidism. A case report]. 194 10

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

Opiates stimulate the growth hormone and prolactin responses to stimuli in non-obese humans. Obese patients, however, show lowered growth hormone and prolactin responses and raised beta-endorphin levels. We therefore investigated the effect of the opiate antagonist naloxone on the stimulated growth hormone and prolactin secretions in a controlled double-blind study in obese patients. All patients received 200 micrograms TRH and 0.5 g/kg b.w. arginine together with 2 mg of naloxone or placebo i.v. in a randomized sequence. The TRH- and arginine-induced increases in prolactin and growth hormone were significantly greater after administration of naloxone (p less than 0.05). Naloxone also produced a significant increase in ACTH, cortisol and beta-endorphin when compared with placebo. TSH, triiodothyronine, thyroxine, insulin, glucagon and blood glucose showed no significant differences between both days of the trial. The effect of naloxone on growth hormone and prolactin secretions in obese humans can thus be regarded as a partial normalization. We therefore conclude that the hypothalamic regulatory disturbance of growth hormone and prolactin secretions in the obese could be caused by raised opiate levels.
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PMID:Naloxone increases the response of growth hormone and prolactin to stimuli in obese humans. 303 2

Nine patients (4F, 5M) aged 12-17 years with "fear of obesity" were studied with a sequential stimulation test utilizing insulin, LRH, TRH, and L-dopa. The comparative groups were nine female with classic anorexia nervosa, five males with undifferentiated nutritional dwarfing, and nine children (1F, 8M) with constitutional growth delay. The serum TSH, glucose, cortisol, somatotropin, prolactin, LH, and FSH were sampled periodically over 2 hours. Basal T3, T4, transferrin, and Somatomedin-C levels were also obtained. The "fear of obesity" patients did not have any pituitary function changes that were unique. These patients, as well as the comparison groups, revealed a delayed TSH response in proportion to the weight deficit which, when expressed as an integrated response, correlated well to the weight deficit for height (P less than 0.001) and to the ability to recover from hypoglycemia (p less than 0.001). The Somatomedin-C level was low and correlated to the T3 level (p less than 0.05) and not correlated to the elevated Somatotropin levels. The pituitary response to combined stimulation in patients with fear of obesity was determined to be a component of the spectrum starting at normal and proceeding to the extreme undernutrition of anorexia nervosa. Pituitary responsiveness, therefore, changes not as a function of the etiology of the malnutrition, but simply as a function of its severity.
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PMID:Pituitary-hypothalamic response in adolescents with growth failure due to fear of obesity. 310 48

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


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