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)

Particular aspects of plasma ACTH radioimmunoassay are examinated. The results obtained with this method in adrenocortical diseases (Addison's disease, Cushing's syndrome, congenital adrenal hyperplasia) are reported and clinical value in etiological diagnosis of Cushing's syndrome is outlined. Moreover the results obtained in other syndromes of endocrinologic interest (massive obesity, Turner's and Klinefelter's syndromes, Laurence-Moon-Biedl syndrome, true precocious puberty, primary hypothyroidism, hypopituitary dwarphism) are reported and discussed.
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PMID:[Technical notes and clinical use of radioimmunologic determination of plasma ACTH]. 17 22

Lipid mobilizing substances (LMS) are present in the hypothalamus and pituitary of mammals and probably are involved in the central neural control of obesity. Most of these have direct lipolytic effects, like lipid mobilizing factor (LMF) and LH-RH from the hypothalamus as well as lipotropin (LPH), melanocyte-stimulating hormone (MSH), corticotropin (ACTH), and growth hormone (GH) from the pituitary gland. Some of the substances, like GH-release inhibiting hormone (GH-RIH), affect lipolysis by secondary actions on pancreatic hormones such as insulin and glucagon. Other hypothalamic hormones, like GH-releasing hormone (GH-RH) may influence lipolysis secondarily through the pituitary hormones (e.g. GH) whose release they control. Regardless of how lipid mobilization is affected, investigations into the problem of obesity should take these LMS into consideration.
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PMID:Lipid mobilizing hormones of the hypothalamus and pituitary. 17 3

A rare case of the Cushing syndrome, due to bilateral adrenal hyperplasia is described. Because of generalized obesity, normal height, normal bone age and family history of obesity, a boy 10 years of age had at first been misdiagnosed as simple obesity. A reduction in height velocity, advancement of bone age and development of precocious pseudopuberty led to a more detailed biochemical investigation and to the correct diagnosis. The clinical picture can be misleading in the differential diagnosis of Cushing's disease versus simple obesity. From a comparison of reports on pediatric Cushing's syndrome, it is obvious that in most pediatric cases fat distribution differs from that of adult Cushing's syndromes. Stunted growth is reported to be more frequent, but normal and excessive height in Cushing's syndrome is not uncommon. In adrenal hyperplasia a retardation of bone age is usually expected. Interpretation of endocrine functions must take into account that simple obesity leads to secondary endocrinopathies, which are similar to the findings in Cushing's syndromes. Plasma cortisol at midnight and 12 hourly excretion of free cortisol in urine as well as overnight Dexamethasone suppression of morning plasma cortisol are judged to be good screening parameters. Plasma ACTH assays can help in the initial diagnosis and are mandatory during the follow up for an early detection of Nelson's syndrome.
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PMID:Cushing's syndrome or obesity. Bilateral adrenal hyperplasia in a boy 10 years of age. 17 22

The basal plasma level of GH, TSH and ACTH and the reserve capacities of the adenohypophysis in the secretion of these hormones was investigated radioimmunologically in 80 patients with excessive weight (from 15.3% to 180.0%) and a group of healthy subjects. It is shown that obesity is accompanied by diverse changes of the anterior pituitary GH, TSH and ACTH functions, which may be explained by their varied participation in the fatty metabolism. The pituitary somatotrophic function is weakened in obese subjects and its disorders advance with increase of the grade of obesity. Reduced pituitary thyrotrophic function in obesity causes weakening of thyroid function; disorders of the thyroid regulation occur at the hypothalamic level. The increased blood plasma concentration of ACTH in obese subjects has a compensatory character. The reserve capacities of the adrenocorticotrophic function of the pituitary are diminished in obestiy. Disturbances of the anterior pituitary GH, TSH and ACTH functions show a single-direction character both in alimentary-constitutional and in hypothalamic obesity.
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PMID:Somatotrophic, thyrotrophic and adrenocorticotrophic functions of the anterior pituitary in obesity. 19 33

The presenting signs, symptoms, roentgenographic findings, endocrine evaluations, treatment, and results in 68 cases of presumed pituitary adenomas treated over an 18-year period are discussed. The most common symptoms were headache, acromegalic changes, visual symptoms, and amenorrhea. Most common physical findings were obesity, acromegaly, and visual field defects, usually bitemporal hemianopsia. Roentgenographic evidence of sellar erosion was almost universal but angiography and pneumoencephalography were required to evaluate suprasellar extension. Brain scan was not considered a particularly useful diagnostic tool. Endocrine status was best evaluated by a battery of tests including 17-OH, 17-KS, T3, T4, PBI, ACTH stimulation, and FSH and STH levels. (Prolactin levels are currently being obtained, also). Surgical specimens were obtained in 29 patients, with subsequent diagnoses of 22 chromophobe adenomas, five eosinophilie adenomas, one cystic adenoma, and one necrotic tumor. All five eosinophilic tumors came from acromegalic patients. Patients treated by operation alone or operation followed by radiotherapy generally had less "medical morbidity" than did patients who received radiotherapy alone.
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PMID:Review of 18 years' experience with pituitary tumors. 19 48

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

Ectopic ACTH syndrome is a clinicopathologic condition produced by certain tumors which release hormone that is indistinguishable from ACTH. It orginates the chemical and clinical anomalies characteristic of Cushing's syndrome by its action on the adrenal glands. The tumors may be present in any organ, though they are most frequently found in the lungs, thymus, pancreas or gastrointestinal tract. They may be benign or malignant, though usually the latter. Secretion of the hormone is completely autnomous; it is release in a way similar to that of the hypophysis. Not infrequently other hormones besides ACTH are also produced, such as MSH, serotonin, and CRF. Ectopic ACTH is of higher molecular weight than hypophyseal ACTH, which suggest it may be comprised of the latter bounded covalently to a peptide. The clinical course is rapid, so that not all of the symptoms of Cushing's syndrome develop. Moon face, osteoporosis, and obesity are typically lacking; melanodermia and hypokalemic alkalosis ofter appear. Laboratory data include an increase in ACTH and cholesterol concentrations, disappearance of the nictameral rhythm, and an increase in urinary excretion of 17-hydroxycorticoids and 17-ketosteroids. Stimulation and supression tests are abnormal. The prognosis is poor and the only possible treatment is a complete surgical removal of the tumor. Irradiation or chemotherapy could be applied as well as the correction of the adrenal hyperfunction by the administration of drugs or by total bilateral adrenalectomy.
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PMID:[Ectopic ACTH syndrome (author's transl)]. 22 77

Obese patients who voluntarily reduce to a normal weight may develop secondary amenorrhea. Six young women who dieted to lose from 13 to 50 pounds, including four from an obese weight, were evaluated because of absent cervical mucus ferning, hypoestrogenic vaginal smears, and failure to have withdrawal menses from a progestogen. Serum FSH values were normal in all, while four had normal serum LH and two had low serum LH levels. T4 and/or T3 uptake was normal in all. The pituitary-adrenal axis was apparently intact since baseline urinary steroids were normal as was the response to both ACTH and metyrapone. Fasting serum growth hormone was markedly elevated in two and slightly elevated in three, with the other patinet demonstrating an unusually high response to glucagon/propranolol in the 30 minute specimen. These endocrine findings are similar to those observed in patients with anorexia nervosa, but the weight loss is entirely voluntary and there was no associated psychiatric abnormality.
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PMID:Amenorrhea secondary to voluntary weight loss. 48 81

A 52-year-old woman was admitted to our hospital for further examination of central obesity, hypertension and hirsutism suggesting Cushing's syndrome. Hirsutism had been remarkable for two years, and muscle weakness of the lower extremities gradually developed during the past year. CT scan revealed a tumor in the left adrenal gland which was 1 cm in diameter, round, well-circumscribed, homogeneous and not enhanced. Endocrine data disclosed increased urinary 17-OHCS (11.5-16.4 mg/day) and elevated plasma ACTH (125 pg/ml) and cortisol (19 micrograms/dl) with a lack of diurnal rhythm. Administration of the single-dose dexamethasone (1mg) did not suppress plasma cortisol. However, consecutive administration of either 2mg or 8mg of dexamethasone for 2 days suppressed both plasma cortisol and urinary 17-OHCS. Administration of metyrapone raised both urinary 17-OHCS and plasma ACTH levels. Rapid ACTH test resulted in a hyperresponse of plasma cortisol. CRF injection raised plasma ACTH and cortisol. Bilateral adrenal glands were well demonstrated by 19-iodocholesterol (I-131) scintigraphy during the administration of dexamethasone. MRI with Gd-contrast revealed a microadenoma in the sella turcica. With the diagnosis of Cushing's disease, the microadenoma was removed by the transsphenoidal approach and adrenal function was normalized. However, the left adrenal tumor remained on CT scan but was not demonstrated by scintigraphy. These findings indicate that this is a very rare case of Cushing's disease which was associated with an unilateral non-functioning adrenal tumor.
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PMID:[A case of Cushing's disease associated with a non-functioning adrenal tumor]. 129 36

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


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