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

The metabolic mechanism for increased circulating free fatty acids in post-menopausal women with metastatic breast cancer was investigated. Hormone and metabolic response to glucose and growth hormone were compared to cancer patients and control subjects; thyroid, adrenal and pituitary function were evaluated. The results of these studies indicated that breast cancer patients had glucose intolerance and delayed and prolonged insulin secretion, increased basal growth hormone levels and insensitivity of adipose tissue to growth hormone. Cortisol and protein-bound iodine levels were normal and there was no lipolytic factor in the sera of breast cancer patients. The changes observed in breast cancer patients were not attributable to age, obesity, inanition or stress. These metabolic abnormalities may characterize host susceptibility to breast cancer or be effects of tumor.
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PMID:Metabolic parameters in women with metastatic breast cancer. 4 95

1. Male rats were injected daily for 5 days with 0.15m-NaCl, corticotropin, cortisol or l-thyroxine and the rates of glycerolipid synthesis were measured in the livers after intraportal injection of [(14)C]palmitate and [(3)H]glycerol. 2. Injection of all three hormones decreased the rates of body-weight gain. 3. Cortisol treatment increased the weight of the liver relative to body weight. 4. Thyroxine treatment increased the relative rate of triacylglycerol synthesis from [(3)H]glycerol and decreased the relative accumulation of (3)H and (14)C in diacylglycerol. It did not significantly alter the accumulation of these isotopes in phosphatidate nor the activity of the soluble phosphatidate phosphohydrolase in the total liver. However, this activity increased by 1.5-fold when expressed relative to the soluble protein of the liver. The increased triacylglycerol synthesis appears to be related to a general increase in the turnover of fatty acids in the liver. 5. Treatment with cortisol and corticotropin increased the relative rate of triacylglycerol synthesis from [(3)H]glycerol, decreased the accumulation of (3)H in phosphatidate and increased the flux of both isotopes from phosphatidate to diacylglycerol. This appeared to be caused by the increased activity of the soluble phosphatidate phosphohydrolase that was observed in the livers of the cortisol-treated rats. 6. It is proposed that cortisol could be directly or indirectly involved in increasing the activity of hepatic phosphatidate phosphohydrolase in starvation, diabetes, laparotomy, subtotal hepatectomy, liver damage, ethanol feeding and in obesity. This enzyme adaptation could contribute to the potential of the liver to increase its synthesis and accumulation of triacylglycerols or to secrete very-low-density lipoproteins.
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PMID:The effects of cortisol, corticotropin and thyroxine on the synthesis of glycerolipids and on the phosphatidate phosphohydrolase activity in rat liver. 21 53

Insulin resistance is the cornerstone for the development of non-insulin-dependent diabetes mellitus (NIDDM). Free fatty acids (FFAs) cause insulin resistance in muscle and liver and increase hepatic gluconeogenesis and lipoprotein production and perhaps decrease hepatic clearance of insulin. It is suggested that the depressing effect of insulin on circulating FFA concentration is dependent on the fraction derived from visceral adipocytes, which have a low responsiveness to the antilipolytic effect of insulin. Elevated secretion of cortisol and/or testosterone induces insulin resistance in muscle. This also seems to be the case for low testosterone concentrations in men. In addition, cortisol increases hepatic gluconeogenesis. Cortisol and testosterone have "permissive" effect on adipose lipolysis and therefore amplify lipolytic stimulation; FFA, cortisol, and testosterone thus have powerful combined effects, resulting in insulin resistance and increased hepatic gluconeogenesis. All these factors promoting insulin resistance are active in abdominal visceral obesity, which is closely associated with insulin resistance, NIDDM, and the "metabolic syndrome." In addition, the endocrine aberrations may provide a cause for visceral fat accumulation, probably due to regional differences in steroid-hormone-receptor density. In addition to the increased activity along the adrenocorticosteroid axis, there also seem to be signs of increased activity from the central sympathetic nervous system. These are the established endocrine consequences of hypothalamic arousal in the defeat and defense reactions. There is some evidence that suggests an increased prevalence of psychosocial stress factors is associated with visceral distribution of body fat. Therefore, it is hypothesized that such factors might provide a background not only to a defense reaction and primary hypertension, suggested previously, but also to a defeat reaction, which contributes to an endocrine aberration leading to metabolic aberrations and visceral fat accumulation, which in turn leads to disease.
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PMID:Metabolic implications of body fat distribution. 177

Adipose tissue distribution in man is dependent on genetic and environmental factors. The total and regional masses of adipose tissue are dependent on the number of adipocytes as well as their degree of filling with depot fat. Currently available evidence does not suggest a specific regional regulation of fat cell multiplication in subcutaneous depots, which instead seems to occur at a certain critical degree of filling of available adipocytes. The control of the rate of filling of adipocytes then seems to be the main factor determining the local, regional mass of adipose tissue. This in turn is regulated by the balance between the lipid accumulating and mobilization processes. The steroid hormones exert major permissive effects on these processes. It seems likely that the resulting effect of the rate of secretion of various steroid hormones, and the local density of their specific receptors, decide the regional distribution of body fat. Physiological and clinical situations with defined differences in these regulatory factors would then be expected to have characteristically different adipose tissue distribution. Sex differences include a larger subcutaneous adipose tissue in women than men, explainable at least partly by a depot in the gluteal-femoral region in women, which is essentially absent in non-obese men. Men on the other hand seem to have a larger proportion of their adipose tissue organ localized intra-abdominally. In addition, the gluteal-femoral fat cells are specifically enlarged in women, and have a higher lipoprotein lipase activity. While the larger adipose tissue in non-obese women may well be genetically linked, the specific characteristics of the gluteal-femoral adipocytes are most likely regulated by female sex steroid hormones. Another apparent sex difference is the ability of women to protect visceral depots from fat accumulation up to a certain degree of obesity, while men deposit excess fat in this region in parallel with other depots. This might, at least partly, simply be explainable by the smaller 'available space' in male than female adipose tissue. It should be emphasized that the effects of sex steroid hormones on the regulation of adipocyte metabolism occur only in concert with cortisol, which is always present. Cortisol itself expresses lipoprotein lipase activity as well as beta-adrenergic receptors (BARs), and probably has additional effects, not yet revealed. The net effect seems, however, to be lipid accumulation as seen in the apparently glucocorticoid receptor (GR) dense visceral adipose tissue in conditions of glucocorticoid excess, such as Cushing's syndrome. The effects of the sex steroid hormones should be regarded against this background.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adipose tissue distribution and function. 179 41

Patients with simple exogenous obesity are characterized by increased B-endorphin (B-EP) plasma levels, despite normal ACTH and B-Lipotropin (B-LPH). To evaluate the origin of such an hyperendorphinemia, 42 obese patients were submitted to a short overnight dexamethasone suppression test (DST: 1 mg at 23:00 h). Blood samples were taken in basal conditions and 9, and 17 h after DST. The same procedure was applied in 12 healthy, normal weight volunteers. In further five patients, 0.5 mg per 4/die were given. B-EP was measured by radioimmunoassay (RIA) after silicic acid extraction and Sephadex G-75 column chromatography. ACTH and Cortisol were measured by direct IRMA and RIA, respectively. Basal B-EP levels of patients (24.2 +/- 16.5, fmol/ml, M +/- SD) were double than in normal weight controls (10.8 +/- 4.6), while ACTH and cortisol fell in the normal range. ACTH and cortisol were significantly reduced by DST in both patients and controls, while B-EP in patients did not. Cortisol, however, was not suppressed in 7 patients (16%). At 08:00, the suppression of B-EP in controls was 49.0 +/- 18.4%, while in obese patients it was only 21.2 +/- 38.8% (p less than 0.01). However, patients with weight excess below 50% normally suppressed B-EP (41.6 +/- 15.3%), while those with weight excess over 75% did not (11.3 +/- 47.5%). The doubling of dexamethasone intake does not lead to a suppression of plasma B-EP in these last patients. These data indicate the existence of neuroendocrine abnormalities in the hypothalamus-pituitary-adrenal axis of obese patients and suggest that their hyperendorphinemia originates outside the anterior pituitary.
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PMID:Plasma B-endorphin resistance to dexamethasone suppression in obese patients. 283 30

To study the role of opioid peptides in human obesity, plasma beta-endorphin (beta EP), beta-lipotropin (beta LPH), and cortisol resting values, circadian rhythms, and responses to hypoglycemia were studied in 6 prepubertal and 6 pubertal obese adolescents (at least 40% above ideal body weight) and in 10 normal subjects matched for age, sex, and pubertal development. Baseline plasma beta LPH and beta EP concentrations in both obese children and adolescents were twice as high as those in normal controls, while cortisol levels were not different. Cortisol, beta EP, and beta LPH levels had a clear circadian rhythmicity in all subjects, with the exception of obese pubertal boys whose plasma beta EP concentrations were constant throughout the day. After insulin administration, the fall in blood sugar was similar in all groups. Plasma cortisol and beta EP responses were similar in both obese and normal prepubertal subjects. In obese pubertal adolescents, beta EP did not increase significantly after hypoglycemia, although it did increase in normal weight pubertal subjects. In normal prepubertal subjects, the circadian rhythms of beta EP and beta LPH secretion and release induced by hypoglycemia suggest the presence of a well developed neuroendocrine control of proopiomelanocortin-related peptide secretion. In prepubertal obese children, the increased plasma beta EP and beta LPH levels with the maintenance of their circadian rhythm and responsivity to hypoglycemia suggest overactivity of anterior pituitary secretion. In obese adolescents, in spite of the normal rhythm of beta LPH and cortisol, beta EP levels did not change throughout the day, thus suggesting beta EP secretion from nonpituitary sources in these subjects. The present study indicates a possible direct role for hyperendorphinemia in the induction of overeating in obese children and adolescents.
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PMID:Hyperendorphinemia in obese children and adolescents. 293 22

Plasma B-Endorphin (B-EP), Growth Hormone (GH) and cortisol response to 100 mcg/m2 b.s., i.v. clonidine (an alpha 2-adrenergic agonist) were evaluated in 17 normal weight children (8 prepubertal and 9 pubertal) and in 15 children with simple exogenous obesity (7 prepubertal and 8 pubertal, weight excess ranging from 29% to 97%). All the hormones were measured by radioimmunoassay either directly in the plasma (GH and cortisol) or after extraction and chromatography (B-EP). Obese prepubertal and pubertal children showed basal B-EP levels significantly higher than in controls and no differences were found in GH and cortisol levels. While in controls clonidine stimulated a significant release of plasma GH and B-EP in obese patients, irrespective of pubertal development, no changes were found. Cortisol levels decreased in both groups. These data suggest an impaired adrenergic control of GH and B-EP secretion in children with simple exogenous obesity.
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PMID:Absent B-endorphin response to clonidine in obese children. 297 Oct 10

Cortisol and growth hormone (GH) responses to a 100 g oral glucose load were measured in 85 Indian patients with non-insulin-dependent diabetes in the young (NIDDY) and 50 reference subjects; in 16 patients and 12 reference subjects the glucagon responses were also assessed. Fasting serum cortisol and plasma glucagon levels were significantly higher in the NIDDY group (P less than 0.001); in contrast, GH levels in the NIDDY patients were significantly lower (P less than 0.01). Plasma glucagon was only significantly suppressed 150 minutes after oral glucose loading in the NIDDY group, in contrast to the reference group, which showed maximum suppression at 90 minutes; at all time intervals plasma glucagon levels were significantly higher in the NIDDY patients. Obesity did not affect fasting plasma glucagon levels. In response to the oral glucose load serum cortisol levels in the NIDDY patients were suppressed in parallel with those in the reference group but remained significantly higher throughout the period of observation at all time intervals. Obese NIDDY patients had higher fasting cortisol levels, but their response to orally administered glucose was no different from that of the NIDDY group as a whole. GH suppression by oral glucose in NIDDY patients was less than that in the reference group, and the rebound rise occurred earlier. Obese NIDDY patients had higher fasting GH levels than their non-obese counterparts, but responses to the glucose load were not different.
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PMID:Cortisol, glucagon and growth hormone responses to oral glucose in non-insulin-dependent diabetes in the young. 675 Aug 13

Effects of physical training on factors associated with diabetes mellitus and its increased risk for cardiovascular disease are reviewed. Plasma insulin levels are decreased by training particularly in obesity and glucose tolerance seems to be improved. Training leads also in general to diminished body fat, but this is not obligatory for the plasma insulin decrease. There are no changes in concentrations of amino acids growth hormone or catecholamines, which can explain the insulin decrease. Cortisol is decreased the days after an acute exercise as well as after training in parallel with the plasma insulin decrease. The cortisol decrease may lead to changes in insulin receptor density in tissues leading to increased insulin sensitivity. The insulin decrease seems to be due to both a decreased production (to about 2/3) and an increased clearance (to about 1/3). Physical training leads to a decrease in plasma triglycerides and to a decrease in blood pressure. All these effects of physical training seem to be beneficial in the treatment of diabetes mellitus.
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PMID:Metabolic effects of physical training. 701 Sep 7

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


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