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)

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

Serum thyroid hormones in childhood obesity are not altered but caloric intake affects monoiodination of T4 to T3 and rT3. Plasma cortisol and urinary free cortisol concentrations are normal. Increase in cortisol production and secretion rate is reflected in increased values of urinary 17-hydroxycorticosteroids. Elevated urinary 17-ketosteroids are caused by increased androgen synthesis accounting for the increased height velocity in obese preadolescents and for the accelerated skeletal maturation. In both sexes earlier onset of puberty is noticed without remarkable alterations in gonadal steroids. Whether altered prolactin concentrations reflect neuroendocrine abnormalities remains unclear. Impairment of growth hormone release in face of normal or high somatomedins is not of clinical significance. Basal and stimulated insulin concentrations are high. Insulin resistance exists because glucose tolerance is simultaneously impaired. This is due to reduction in insulin receptor numbers and post-receptor defects in insulin action. Weight loss is effective in normalizing the above mentioned hormonal defects.
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PMID:[Hormonal findings in obese children. A review]. 330 53

A case-control study was conducted in Los Angeles County, CA, of 75 male breast cancer cases aged 20-74 yr at diagnosis to investigate the role of a number of suspected risk factors. The study involved both interviews and laboratory measurements. Factors under study included fertility and marital history, obesity, alcohol and cigarette consumption, use of drugs known or suspected of causing gynecomastia, family history of breast cancer, history of radiation exposure to the upper body, sex chromatin analysis, serum levels of prolactin, testosterone, estrone, estradiol and sex-hormone-binding globulin, as well as urinary levels of estrone, estradiol, and estriol. Two patients versus no controls tested positive for sex chromatin and were excluded from further analyses. The only statistically significant risk factor identified was greater weight of the cases at age 30; a man who weighed 80 or more kg at age 30 had twice the risk of breast cancer of a man weighing less than 60 kg at that age. Serum estrone levels were positively, and sex-hormone-binding globulin levels were negatively, related to body weight, and we interpret the greater weight of the cases as suggesting that the underlying risk factor is an increased exposure to bioavailable estrogen. None of the differences observed between cases and controls for either the serum or urinary hormone levels was, however, statistically significant and there did not appear to be any large absolute excess of estrogens or deficit of testosterone in the cases. This apparent contradiction may be explained by the fact that there was little difference in weight between the cases and controls at the time of sampling.
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PMID:A case-control study of male breast cancer. 334 11

A 45-year-old man, was admitted for investigation of severe sexual impairment. During 20 years of marriage, he had had no normal sexual intercourse and the couple was childless. Physical examination disclosed a severely obese man (weight 300 kg, height 1.75 m), with a relatively small and invaginated penis and small (5 ml) soft testes. Laboratory examinations disclosed the following: low serum testosterone (1 ng/ml), with a reduced response to HCG (3.8 ng/ml). Sex hormone binding globulin was at the lower limit of normal (0.38 microgram/dl), serum free testosterone was low (0.98% of total testosterone) as well as non-SHBG bound testosterone (22% of total testosterone). Daily total urinary estrogen excretion was increased (107 micrograms), the plasma estrone (78 pg/ml) and estradiol (74 pg/ml) were elevated. The gonadotropins were normal and responded adequately to LRH. Plasma growth hormone was decreased, prolactin, T4 and adrenal steroids were normal and responded normally to stimuli and inhibitors. Chromosomal constitution was 46XY. Thus, in this man the marked obesity produced a significant increase in estrogens which subsequently induced a severe decrease in testosterone and its free counterpart in excessive impairment of sexual function.
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PMID:Severe sexual impairment produced by morbid obesity. Report of a case. 339 34

Obese subjects show a subnormal growth hormone (GH) and prolactin (PRL) release in response to a variety of stimuli. Fenfluramine, an anorexiant drug used in obesity therapy, may have some effects on hypothalamic-pituitary function mediated by serotoninergic stimulation. The present investigation in obese subjects was carried out to study the effects of fenfluramine (60 mg orally) on GH and PRL secretion after intravenous arginine infusion. Ten volunteer obese females were studied and compared with 10 volunteer normal weight controls. In the obese group the GH response to arginine was significantly lower than in control group. Fenfluramine administration restored the subnormal GH response to arginine in obese subjects. The PRL response to arginine in obese women was subnormal. Fenfluramine administration restored the response of PRL to arginine infusion to normal. In conclusion, fenfluramine--under acute circumstances--enhances the hypothalamic-pituitary response to arginine in obese subjects. The decreased GH and PRL output in obese subjects is not due to an absolute hormonal deficiency and this effect of fenfluramine on GH secretion may--due to its lipolysis stimulation--be useful in obesity treatment.
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PMID:Effect of fenfluramine on growth hormone and prolactin secretion in obese subjects. 343 16

Four female patients were found to have microadenomas and high prolactin levels, but the symptoms of the syndrome varied among the patients. Three of four patients had overt galactorrhea, obesity, and amenorrhea. One patient was postmenopausal, and another showed menstrual irregularities. Two patients sought medical attention for headaches, and one for visual disturbances. Two patients previously had used psychotropic drugs, and two patients used birth control pills. When tested, all patients had high serum prolactin levels, abnormal sellar tomograms, and the presence of microadenoma of the pituitary was confirmed by computerized tomography.Because of the high incidence of pituitary tumor among these four patients, this study suggests that a complete workup should be done for patients having galactorrhea, amenorrhea, and obesity as a syndrome or as separate entities.
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PMID:Syndrome of galactorrhea, amenorrhea, and obesity as possible indicators of prolactinoma: a case study approach. 380 93

Twelve obese patients and 7 control subjects, age and sex matched, whose weights were greater than 200% of ideal weight and 100% of ideal body weight, respectively, underwent intravenous insulin and thyroid releasing hormone (TRH) tests. Serial prolactin growth hormone, insulin, blood sugar, cortisol, glucagon, thyrotropin stimulating hormone, thyroxine, and triiodothyronine were obtained by RIA. Obese patients showed no significant differences from controls in basal and nadir glucose, basal and peak glucagon, cortisol, and thyroid responses to both tests. Basal insulin levels were higher (36 +/- 9.4 vs 10 +/- 2.3 microU/ml, P less than 0.05) and peak growth hormone responses after insulin were lower in the obese group (6.1 +/- 1.1 vs 12.7 +/- 3.7 ng/ml, P less than 0.05) than in controls. Whereas all control subjects had prolactin responses to both tests, five of 12 obese patients had no responses to insulin. Obese patients had lower prolactin responses at 30 minutes after insulin (5.4 +/- 0.7 vs 12.9 +/- 3.7 ng/ml, P less than 0.05) and lower prolactin responses at 60 minutes after TRH (9.9 +/- 1.7 vs 20.4 +/- 5.9 ng/ml, P less than 0.05). Maximum prolactin responses after TRH were lower in obese patients (9.9 +/- 2.0 vs 28.8 +/- 10.9 ng/ml, P less than 0.05). Maximum prolactin responses after insulin were lower in obese patients (6.2 +/- 4.1 vs 28.9 +/- 18.3 ng/ml). Thus prolactin secretion in childhood obesity is decreased after both stimuli, but more so after IV insulin that TRH, and suggests that, as in adult hypothalamic obesity, neuroendocrine regulation of prolactin release in obese children is impaired.
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PMID:Decreased prolactin secretion in childhood obesity. 391 66

In order to investigate dopaminergic activity in two types of human obesity, childhood- and adult-onset, we have studied the responses of plasma TSH and prolactin to domperidone, a dopamine receptor antagonist, in 12 patients obese since early childhood, 12 patients with adult-onset obesity, and in 12 lean controls. All subjects were females. In childhood-onset obese patients the responses of plasma prolactin and TSH to antidopaminergic stimulation were lower than those of adult-onset obese patients and lean controls. Conversely, the stimulus elicited a normal response of plasma prolactin and an exaggerated response of plasma TSH in adult-onset obese patients. These data indicate the presence of differing dopaminergic tone in the two types of human obesity.
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PMID:Evidence for differing dopaminergic activity in childhood- or adult-onset obesity. 391 73

The responses of pituitary hormones and venous catecholamine concentrations to insulin hypoglycaemia were studied in 12 formerly obese women with familial obesity who had lost about 30 kg by dieting. These responses were compared with those of 10 lean women. The post-obese women showed an exaggerated response in cortisol output but an impaired release of growth hormone. 6 of the post-obese women had in addition both an impairment in prolactin output and a failure to increase their venous noradrenaline concentrations during hypoglycaemia. These results suggest that an alteration in hypothalamic control, displayed by limited responses in pituitary hormone secretion and by reduced sympathetic activity, may be an innate feature of people with familial obesity
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PMID:Altered hypothalamic and sympathetic responses to hypoglycaemia in familial obesity. 612 54

The effect of a single dose of 150 mg depomedroxyprogesterone acetate (DMPA) on pituitary, ovarian, and endometrial function was assessed in relation to the peripheral levels of the compound in 8 women. The levels of DMPA, follitropin (FSH), lutropin (LH), prolactin, estradiol (E2), and progesterone (P) were measured 3 times/week during a pretreatment (control) cycle and then daily during postinjection weeks 14-17, 22-25, and 30-33. An endometrial biopsy specimen was obtained during postinjection weeks 17, 25, and 33. In 3 of 8 subjects the daily hormone assays carried out during postinjection weeks 30-33 indicated anovulatory periods; in these subjects, peripheral blood was drawn daily during postinjection weeks 46-49 and a 4th endometrial biopsy was taken during week 49. Plasma DMPA levels during the 14th postinjection week varied between 0.90 and 2.24 nmol/1, declined gradually, and became undetectable between weeks 17-24 (4 cases) or some time after week 33 (the other 4 cases). No correlation was found between the time when DMPA levels became undetectable and the obesity index.
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PMID:Return of ovulation following a single injection of depo-medroxyprogesterone acetate: a pharmacokinetic and pharmacodynamic study. 623 45


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