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

The contribution of the adrenal gland to the development of the spontaneous syndrome of obesity and diabetes in Yellow-KK (Y-KK) mice was studied. Six-month old Y-KK mice exhibited hyperadrenocorticism and adrenal cortex enlargement. Light microscopic morphometric studies of Y-KK adrenals revealed an expanded volume of the adrenal cortex resulting from hyperplasia of zona fasciculata and reticularis cells. Ultrastructural studies revealed fewer lipid droplets, increased numbers of mitochondria and a more extensively developed Golgi system with zona fasciculata and reticularis cells. This cytological evidence of enhanced steroid biosynthetic and secretory activity was consistent with increased levels of plasma immunoreactive corticosterone. Structural and functional abnormalities of Y-KK adrenals were preceded by the development of obesity, hyperglycaemia and hyperinsulinaemia. It is unlikely, therefore, that the adrenal plays a casual role in the syndrome's pathogenesis, although, hyperadrenocorticism may be in part responsible for an exacerbation of the observed phenomena.
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PMID:Adrenal gland involvement in mice with hereditary obesity and diabetes mellitus. Morphological studies. 46 49

Two patients are described in whom hypercortisolism occurred prepubertally as a consequence of bilateral adrenocortical hyperplasia. In contrast with the manifestations of Cushing's syndrome in adults, these children presented with obesity and reduced stature and no other symptoms. Both patients excreted amounts of urinary 17-OHCS before and during a conventional suppression test with dexamethasone (0.5 mg every six hours) which were within the usual normal range. However, when urinary 17-OHCS excretion was expressed per gram of urinary creatinine or per square meter of surface area, and when the dose of dexamethasone was tailored to body mass (20mug/kg/day) the results were clearly abnormal, as were plasma corticoids and (in one patient) cortisol secretion rate. Resumption of linear growth occurred after bilateral adrenalectomy in both patients and was associated, in the one patient so studied, by a return of hypoglycemia-stimulated increases in plasma growth hormone levels from previously suppressed values to the normal range, and by a slight increase in the fasting plasma somatomedin concentration. The observations suggest that pediatric patients with hypercortisolism are likely to be overlooked when conventional criteria for laboratory diagnosis are used, but can be recognized by the simple diagnostic modifications used in these studies.
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PMID:Hypercortisolism in childhood: shortcomings of conventional diagnostic criteria. 119 38

On account of the increasing number of patients with essential obesity the delimitation of the Cushing-syndrome is of actual importance. Two observations of hypercortisolism in hyperplasia of the adrenal glands are reported on and the differential-diagnostically important parameters are demonstrated. According to our opinion anamnesis and clinical findings give the possibility of making a diagnosis already on a large scale. Analyses of the hormones and special X-ray examinations only serve for the preoperative ascertainment and localisation of the endocrine defective function. With the help of literary data causes and possibilities of treatment of Cushing's syndrome are entered.
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PMID:[Differential diagnosis of essential adiposity and Cushings syndrome]. 119 88

The turnover rate of plasma FFA measured by constant infusion of albumin-complexed labeled palmitate in a group of 16 patients with Cushing's syndrome was significantly lower than in a group of 6 controls. Seven patients reexamined after correction of the hypercortisolism showed a normalization of the plasma FFA turnover rate. By contrast, 7 patients with simple obesity had a normal or increased plasma FFA turnover rate depending on the way this parameter is expressed.
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PMID:Depressed plasma FFA turnover rate in Cushing's syndrome. 124 92

Adrenal tumors are usually diagnosed by clinical symptoms of hormone excess. The increasing use of ultrasound and computed tomography results in the detection of a substantial number of incidentally discovered adrenal tumors. Most of these tumors are nonfunctional adrenocortical adenomas, but a few cases of subclinical cortisol production in "incidentalomas" have been reported. We investigated prospectively the prevalence of autonomous cortisol production in 68 patients (44 females and 24 males, aged 25-90 yr) with adrenal incidentalomas at our institution. As a screening procedure all patients with incidentalomas underwent an overnight dexamethasone suppression test (1 mg). Patients who failed to suppress serum cortisol below 140 nmol/L (5 micrograms/dL) underwent more comprehensive studies (prolonged dexamethasone suppression test, determination of the diurnal rhythm of cortisol secretion in saliva, and CRH stimulation test). Eight patients (12% of all patients with incidentalomas; 5 females and 3 males, aged 25-71 yr) were finally identified as having cortisol-producing tumors, and the findings in these patients were compared with those of overt Cushing's syndrome in 8 patients (8 females, aged 26-50 yr) suffering from cortisol-producing adrenal adenomas. The tumor size of patients with cortisol-producing incidentalomas ranged from 2-5 cm. No specific signs and symptoms of hypercortisolism were present, but arterial hypertension (seven of eight subjects), diffuse obesity (four of eight subjects), and noninsulin-dependent diabetes mellitus (NIDDM; two of eight subjects) were frequently observed. Baseline cortisol levels were in the normal to upper normal range, whereas baseline ACTH levels were suppressed in five of the eight patients. In none of the patients was serum cortisol suppressible by low dose or high dose dexamethasone. The ACTH and cortisol responses to CRH were normal in two, blunted in one, and suppressed in four patients. Unilateral adrenalectomy was performed in seven patients and resulted in temporary adrenal insufficiency in four of them. After surgery, improvement of arterial hypertension, a permanent weight loss in obese subjects, and a better metabolic control of NIDDM were noted in the majority of patients. The following conclusions were reached. Incidentally diagnosed adrenal tumors with pathological cortisol secretion in otherwise clinically asymptomatic patients are more frequently observed than previously assumed. Adrenocortical insufficiency is a major risk in these patients after adrenalectomy. After surgery, hypertension, obesity, and NIDDM may improve. Patients with asymptomatic adrenal incidentalomas, therefore, should be screened for cortisol production by means of an overnight dexamethasone suppression test.
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PMID:Preclinical Cushing's syndrome in adrenal "incidentalomas": comparison with adrenal Cushing's syndrome. 151 73

The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Insulin resistance is a cause for morning hyperglycemia seen in diabetic patients. Other reasons for morning hyperglycemia should be eliminated by performing an insulin response test. Once insulin resistance has been established as the cause of hyperglycemia, a step-by-step process should be used to establish the cause of the insulin resistance. Common causes of insulin resistance include hyperadrenocorticism, acromegaly, hyperthyroidism, and obesity. Hepatic disease, renal insufficiency, and sepsis are other causes of insulin resistance in practice. Less common causes include insulin antibodies, pregnancy, neoplasia, hyperandrogenism, and pheochromocytoma. If the underlying cause cannot be found or resolved, then increased doses of insulin are required to manage the hyperglycemia.
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PMID:Problems in diabetes mellitus management. Insulin resistance. 213 77

Most metabolic disorders of genetically obese Zucker rats are reversed by adrenalectomy and are restored by corticosterone treatment, thus suggesting that a functional hypercorticosteronemic state is involved in the pathogenesis of the obesity syndrome in fa/fa rats. However, the hormone content and morphology of the hypothalamo-pituitary-adrenal axis of this animal model have to our knowledge not yet been described. We, thus, investigated morphologically and morphometrically the hypothalamic regions involved in CRF synthesis and secretion in male fa/fa rats. To ascertain if the brain is selectively or uniformly affected, we studied the main nuclei of the lateral and mediobasal hypothalamus, i.e. arcuate, lateral hypothalamic, and ventromedial nucleus and the parvicellular portion of the paraventricular nucleus. Moreover, after immunocytochemical labeling, we analyzed densitometrically the CRF-bearing axons of the median eminence and the ACTH-containing cells of the anterior and intermediate lobe of the pituitary gland. Finally, we investigated the adrenal glands by qualitative light microscopy. In fa/fa rats most hypothalamic nuclei were structurally changed. Furthermore, hypothalamic CRF and anterior pituitary ACTH contents as well as adrenal weight were increased, the zona fasciculata of the adrenal cortex was hypertrophic, and the ACTH content of the intermediate lobe was reduced. In conclusion, our results demonstrate that the obesity syndrome in genetically obese fa/fa rats is associated with lesions of the hypothalamo-pituitary-adrenal axis consistent with hyperadrenocorticism due to hyperactivity of the whole adrenal axis. Alterations also occur in the hypothalamic nuclei controlling glycemia, insulinemia, and circadian corticosterone secretion.
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PMID:Changes in the hypothalamo-pituitary-adrenal axis of genetically obese fa/fa rats: a structural, immunocytochemical, and morphometrical study. 231 48

A patient with Cushing's syndrome due to ectopic ACTH secretion was treated successfully with the new glucocorticoid antagonist RU 486 [17 beta-hydroxy-11 beta-(4-dimethylamino phenyl) 17 alpha-(1-propynyl)estra-4,9-dien-3-one]. This compound is a 19-nor steroid with substitutions at positions C11 and C17 which antagonizes cortisol action competitively at the receptor level. Oral RU 486 was given in increasing doses of 5, 10, 15, and 20 mg/kg . day for a 9-week period. Treatment efficacy was monitored by assessment of clinical status and by measuring several glucocorticoid-sensitive variables, including fasting blood sugar, blood sugar 120 min after oral glucose administration, and plasma concentrations of TSH, corticosteroid-binding globulin, LH, testosterone-estradiol-binding globulin, and total and free testosterone. With therapy, the somatic features of Cushing's syndrome (buffalo hump, central obesity, and moon facies) ameliorated, mean arterial blood pressure normalized, suicidal depression resolved, and libido returned. All biochemical glucocorticoid-sensitive parameters normalized. No side-effects of drug toxicity were observed. We conclude that RU 486 may provide a safe, well tolerated, and effective medical treatment for hypercortisolism.
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PMID:Successful treatment of Cushing's syndrome with the glucocorticoid antagonist RU 486. 299 27

In this study, we investigated the usefulness of the determination of evening urinary free corticoids/creatinine in samples collected from 20.00 to 24.00 h as a screening test in Cushing's syndrome. In controls (N = 61) the ratio values ranged from 1.1 to 9.4 mumol/mol, whereas in patients with Cushing's syndrome (N = 20), they ranged from 27.5 to 855.5 mumol/mol. However, in 28% of patients with major obesity (greater than 50% overweight) and no hypercortisolism, the ratio values were between 9.4 to 27.8 mumol/mol. A short (10 days) hypocaloric diet induced a decrease in the values in 75% of these patients; the normal range was reached in 50% of them. In addition, the evening urinary free corticoids/creatinine was slightly abnormal in 8 out of 10 patients with incidentally discovered 'silent' adrenal adenomas, whereas it was normal in all 6 with other adrenal masses. In conclusion, evening urinary free corticoids/creatinine is easy to obtain and it reaches a higher sensitivity (100%) and specificity (97%) than the 24 h urinary free corticoids. In the case of borderline values, the presence of overweight should be taken into account.
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PMID:Evening urinary free corticoids: a screening test in Cushing's syndrome and incidentally discovered adrenal tumours. 318 14


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