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)

It is concluded that besides NA, some other hormones (adrenaline, glucagon, growth hormone, ACTH, insulin and adrenal steroids) are also thermogenic. While brown adipose tissue is the most important site of heat during NA thermogenesis, some other organs, namely muscles, also contribute to thermogenesis due to various hormones. Hormones seem to potentiate heat production due to their action in target organs. Humoral thermogenesis not only can compensate the heat loss from the body of cold exposed individuals, but it can also prevent obesity under conditions of an high caloric intake. Some substance, on the other hand, induce a hypometabolic effect (rT3, hibernation trigger, antabolone, bombesin). Additionally, absence of gonadal steroids induce hibernation. Thus, humoral substances contribute both to the control of hyper- and hypometabolic states.
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PMID:Humoral control of hyper- and hypometabolic states. 631 84

A 37-year-old woman presented with acute psychosis and cognitive impairment. Skull x-ray showed an enlarged sella turcica with erosion of the floor. Endocrinologic workup suggested the diagnosis of Cushing's disease and hyperprolactinemia. She had no cushingoid feature, and the only physical sign was mild generalized obesity. She showed a paradoxic response to dexamethasone suppression, and underwent trans-sphenoidal resection of a pituitary macroadenoma. Electron microscopy showed the tumor to be a Crooke's cell adenoma. Results of immunohistochemical staining were positive only for ACTH and beta-endorphin. The neuropsychiatric manifestations resolved after surgery.
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PMID:Occult Cushing's disease presenting with acute psychosis. 671 82

The importance of late-onset congenital adrenal hyperplasia as a cause of hirsutism is controversial. Two of 35 women with a chief complaint of hirsutism met the criteria of 21-hydroxylase deficiency. In one, who presented with hirsutism, oligomenorrhea, obesity, infertility, and enlarged cystic ovaries, the initial diagnosis was polycystic ovarian syndrome. Family data showed that her disorder was autosomal recessive and linked to the histocompatibility leukocyte antigens (HLA), as in the classic form of congenital adrenal hyperplasia. Carriers were thus detectable by HLA typing. Thus late-onset congenital adrenal hyperplasia appears to be an allelic variant of congenital virilizing adrenal hyperplasia with a milder enzymatic defect. The diagnosis cannot be made clinically because the disease has the same presentation as idiopathic hirsutism or polycystic ovarian disease. Basal plasma 17-hydroxyprogesterone levels, unlike in classic congenital adrenal hyperplasia, can be normal, and an ACTH stimulation test or sequential measurements of plasma 17-hydroxyprogesterone throughout the day may be needed to show the abnormality. The incidence among hirsute women is estimated to be 6% to 12%, and the calculated gene frequency for the allele coding for attenuated expression of 21-hydroxylase deficiency is 0.015 to 0.057.
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PMID:Late-onset 21-hydroxylase deficiency mimicking idiopathic hirsutism or polycystic ovarian disease. 697 82

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

Individual features of the endocrine system were studied in 26 healthy men, divided into 2 groups, according to the characteristics of EEG, electrocutaneous thresholds and the time response (TR) upon sound signals of 40 to 120 decibels. The subjects of the 1st group were characterized by the high energy of EEG delta- and theta-rhythms, low energy of alpha-rhythm, low thresholds and TR40 : TR120 ratio. The patients of the 2nd group had the opposite parameters. In both groups the blood plasma and urine catecholamine content, ACTH, TTH, 11-hydroxycorticosteroids, cortisol, aldosterone, thyroxine, triiodothyronine, testosterone and plasmatic insulin were determined by means of spectrofluorometry and radioimmunoassay. The elevation of the cortisol level after ACTH injection and of the TTH concentration following thyroliberin administration were investigated. Two polar variants of the endocrine system organization were revealed. The patients of the 1st group had an elevated activity of the sympathico-adrenal, hypophyseal-adrenal system and insular apparatus, comparatively lowered activity of the hypophyseal-thyroid system and gonads. The subjects of the 2nd group demonstrated an opposite character of the endocrine system. It is suggested that the individual peculiarities of the human endocrine system promote the development of obesity, Icenko-Cushing's disease, hypertension, thyrotoxicosis, acromegaly and bronchial asthma.
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PMID:[Individual characteristics of the organization of the human endocrine system]. 712 44

We are presenting a series of 23 patients with Cushing disease selected from a larger study in which the ectopic production of ACTH (paraneoplastic or tumoral), adrenal adenoma or carcinoma were discarded. Sixteen were female and seven male. Diagnosis was fundamentally realized by clinical manifestations derived from hypercortisolism (obesity, muscular atrophy, diabetes, osteoporosis or polyglubulia). The polytomography demonstrated a deformed sella in 19 patients. Endocrine exams showed an alteration in rhythm of Cortisol and elevated levels of urinary metabolites. Others exams, Liddle Test, Metopirona Test, or stimulation of exogenic ACTH did not always permit diagnosis of pituitary adenoma. Plasmatic dosage of ACTH is the best test although results did not always agree with clinical manifestations. In each case we performed clinical treatment in preparation for surgery and later selective removal of adenoma or total pituitary ablation by transphenoidal approach. Of 21 patients, we found an adenoma during surgery in 15; the other 6 on whom we performed a total hypophysectomy, the pathological study showed an adenoma in 5 and a hyperemic gland with thick capillaries in 1. Another type of treatment was used on 2 due to their age. Nine patients were given post-operative radiotherapy. We conclude that microsurgery by transphenoidal approach offers the best possibilities for patients with Cushing disease.
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PMID:[Surgical treatment in Cushing's disease (authors' translation)]. 731 90

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.
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PMID:Cushing's syndrome: problems in diagnosis. 745 63

Dehydroepiandrosterone (DHEA) has been reported to exert antiglucocorticoid activity. When administered to obese, hypercorticosteronemic Zucker rats, it causes a diminution of food intake and a reduction in their rate of weight gain. This experiment was conducted to evaluate whether this biologic effect could be ascribed to chronic adrenal insufficiency. Obese and lean Zucker rats were treated with DHEA as a food supplement for 28 days. Upon sacrifice, organ weights and serum chemistries were measured, along with neurotransmitter levels in regions of the hypothalamus. Results showed that although the obese animals gained weight more slowly, had lower insulin levels, and ate less, their serum glucose, corticosterone, and ACTH levels were not different from control. Hypothalamic neurotransmitters in the obese rat were unaffected by chronic DHEA treatment. We concluded that, although DHEA clearly affects Zucker weight gain, it does not induce chronic adrenal insufficiency.
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PMID:The effect of DHEA given chronically to Zucker rats. 753 42

We report the case of a 17-year-old girl presenting short stature (height 149 cm, below the 3rd percentile), obesity (weight 83.5 kg, body mass index 37 kg/m2) and secondary amenorrhea, in whom endocrinological evaluation disclosed an absolute lack of GH responsiveness to both suprapituitary challenges and repetitive growth hormone releasing hormone administration together with failure of plasma gonadotropins and PRL, low under basal conditions, to rise in response to GnRH and insulin-hypoglycemia, respectively. In contrast, basal and stimulated TSH and ACTH secretions were normal. Radiological examination of the skull revealed virtual absence of the pituitary fossa due to the lack of sellar cavum and dorsum, while magnetic resonance was unable to detect any pituitary tissue. A mucosal cleft of the nasopharynx, compatible with a pharyngeal hypophysis, was disclosed at endoscopy. This is an unusual case of developmental abnormality including lack of formation of the sella turcica and incomplete caudal migration of the embryonal anterior pituitary, resulting in ectopically located--likely pharyngeal--pituitary tissue. In view of the occurrence of spontaneous menarche and of a growth impairment less severe than one would expect considering the degree of GH deficiency, it is conceivable that the ectopic pituitary tissue has lost, in time, some of its secretory ability.
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PMID:Abnormal development of the sella turcica and lack of pituitary visualization in a patient with partial hypopituitarism. 759 30

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55


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