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

The authors report the hormonologic characteristics of 20 obese and hirsute women meeting the criteria for adrenaltype hyperandrogenism, suppressible by dexamethasone, without hyperprolactinemia and without any late developing partial enzyme block appearance. The laboratory profile of these women differed from that of a group of women with type 1 polycystic ovaries syndrome. In this same group obese women in whom LH/FSH ratio was below 1, there was evidence under baseline conditions of a moderate increase in testosterone and delta 4-androstenedione in relation to increased plasma levels of DHA and SDHA, plasma delta 4 and delta 5-androgen levels falling precipitalely during the dexamethasone suppression test. The ACTH stimulation test revealed greater reactivity for 17 hydroxy-pregnenolone (p < 0.001) and less for 21-deoxycortisol than in the control group of normal women (p < 0.01). The essentially adrenal origin of plasma hyperandrogenism in certain cases of obesity is discussed. Insulin could increase adrenal sensitivity to ACTH and its possible action in vivo on the activity of adrenal enzymes requires clarification. The accumulation of certain androgens in the adrenal cortex could also be responsible for dysregulation of 3 beta ol-dehydrogenase and 11-hydroxylase.
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PMID:[Critical study of the characterization of hyperandrogenism in a group of obese women]. 853 5

Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) levels were determined in morning specimens from 659 fasting postmenopausal women who were not using estrogen therapy or antidiabetic medication. All women had concurrent oral glucose tolerance tests and measurements of body mass index (BMI) and waist-hip ratio (WHR). DHEA levels were weakly and inversely associated with BMI but not with WHR or glucose tolerance status. DHEAS levels were not associated with BMI but were positively associated with WHR, diabetes, and impaired glucose tolerance. In analyses adjusted for or stratified by WHR, the DHEAS association with abnormal carbohydrate tolerance was reduced but still independent of fat distribution. Because this was a cross-sectional study, it was not possible to determine whether DHEAS levels were raised by central obesity or vice versa. At a minimum, these data strongly suggest that the positive association of DHEAS with both central obesity and abnormal glucose tolerance does not support the thesis that DHEAS protect against diabetes or obesity in older women as had been suggested by animal studies.
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PMID:Dehydroepiandrosterone, dehydroepiandrosterone sulfate, obesity, waist-hip ratio, and noninsulin-dependent diabetes in postmenopausal women: the Rancho Bernardo Study. 855 Jul 94

Dehydroepiandrosterone sulfate (DHEA-S) is the most abundant circulating adrenal steroid in man, yet its physiologic role and that of its parent compound DHEA are unknown. Age-related decreases in DHEA in association with increases in obesity, insulin resistance, and atherosclerosis are well known. Recent investigations in lower mammals (which do not secrete DHEA) have suggested that DHEA (or its metabolites) may function as an antiobesity agent in these models of obesity independent of food intake. Proposed mechanisms for the decrease in fat mass and lower weight gain when DHEA is given orally include increases in futile cycling and peroxisomal beta-oxidation and decreases in de novo lipogenesis. Alterations in the availability of reducing equivalents for lipid synthesis do not appear to explain this decrease. Changes in pancreatic insulin secretion or insulin sensitivity may also be responsible for some of these effects. Studies in humans have failed to demonstrate a beneficial effect of DHEA on body composition or energy expenditure at either pharmacologic or physiologic replacement doses for 1-3 months. Administration of DHEA to men or women has also not been shown to alter insulin sensitivity as measured by the minimal model or the euglycemic clamp technique. The effect of DHEA on peroxisomal beta-oxidation and de novo lipogenesis is not known. We conclude that a significant role for DHEA in the pharmacologic treatment of human obesity is unlikely.
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PMID:Dehydroepiandrosterone and body fat. 869 65

Zucker rats are a frequently used model in obesity research. Dehydroepiandrosterone (DHEA) reduces their rate of weight gain and caloric consumption. So far, most studies have been conducted while the animals consume laboratory rodent chow, which is low in fat. In the experiments of this communication, Zucker rats were offered fat as a food choice. The goal was to determine how the consumption of fat would affect their weight gain and what effect DHEA would have on macronutrient selection. It was found that Zucker rats both male and female, lean and obese selected nearly 40% of their calories as fat when allowed to choose from nearly pure carbohydrate, protein, and fat foodstuffs. Consuming these three macronutrient diets they ate more calories and gained more weight than chow-fed controls over short periods of time. DHEA administered as an intraperitoneal injection decreased caloric intake of Zuckers. This decrement was quantitatively most important on fat intake. DHEA also prevented weight gain. It is concluded that the availability of fat food affects weight gain in Zucker rats and that DHEA modifies the selection of food such that Zucker rats eat less fat.
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PMID:Effect of DHEA on macronutrient selection by Zucker rats. 877 58

The objective was to study the pathophysiology of the dyslipidaemia in polycystic ovarian syndrome (PCOS) patients, and to determine how it is related to hyperinsulinaemia, hyperandrogenism and dehydroepiandrosterone sulphate (DHEA-S) concentrations. The lipoprotein lipid profile, anthropometric measurements, endocrine profile and the presence of insulin resistance were evaluated in 31 PCOS patients and 20 age-matched healthy women, who served as controls. PCOS patients had higher fasting insulin concentrations, higher body mass indexes (BMI) and were hyperlipidaemic, with higher total cholesterol, low density lipoprotein (LDL) and triglyceride (TG) concentrations. There were no relationships between plasma lipids and anthropometric variables in the patient group as a whole. Insulin-resistant (IR) and non-IR (NIR) PCOS patients were then evaluated separately. Obesity with marked hyperandrogenism were the predominant features in patients with IR. NIR patients were not obese and had significantly less hyperandrogenism. The adrenal androgen DHEA-S was at the upper limit of its normal range in both groups. However, both PCOS subgroups exhibited similar significant abnormalities in terms of their lipid parameters. Insulin and DHEA-S concentrations were positively correlated with total cholesterol, LDL and TG, and negatively correlated with high density lipoprotein, in IR patients. In NIR subjects, insulin was not correlated with any of the lipids and DHEA-S was negatively related to cholesterol and LDL. Anthropometric variables were related to lipids in only the NIR patients. Thus PCOS subjects as a group exhibit dyslipidaemia, characterized by increased total cholesterol, LDL and TG concentrations. When divided into IR and NIR subjects, there were no differences in the degree of lipid abnormalities, despite significant variations in the BMI and androgen status. Thus, in PCOS subjects, dyslipidaemia may occur irrespective of insulin resistance. Insulin and DHEA-S concentrations were positively correlated with an atherogenic lipid profile in the IR group only. As distinct from syndrome X when IR was present, dyslipidaemia was not related to body weight or the waist:hip ratio. In the NIR group there was no relationship between lipids and insulin; DHEA-S, on the other hand, was negatively related to cholesterol and LDL concentrations. Thus, dyslipidaemia in PCOS patients may occur irrespective of insulin resistance, and may have different metabolic aetiologies depending on DHEA-S metabolism. It remains to be seen whether the two types of PCOS are associated with different risks for ischaemic heart disease.
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PMID:Dyslipidaemia in polycystic ovarian syndrome: different groups, different aetiologies? 892 Oct 52

Dehydroepiandrosterone (DHEA) is an adrenal steroid with chemoprotective effects against a wide variety of conditions including cancer, obesity, diabetes, and cardiovascular disease. However, DHEA is also a carcinogen in laboratory animals, possibly through its function as a precursor of sex steroids or peroxisome proliferation. The structural analog 16 alpha-fluoro-5-androsten-17-one (8354) has been reported to have enhanced chemopreventive activity without the steroid precursor and peroxisome proliferating effects of DHEA. This study compares DHEA and 8354 in rainbow trout, a species that is resistant to peroxisome proliferation but is highly susceptible to the carcinogenic and tumor enhancing effects of DHEA. Trout were exposed as fry to aflatoxin B1 (AFB1) or given a sham exposure, then were fed diets containing 444 ppm DHEA or 8354 for 6 months. Postinitiation treatment with DHEA significantly increased liver tumor incidence, multiplicity, and size compared to initiated controls. The analog 8354 slightly increased tumor incidence (p = 0.06) but had no effect on multiplicity or size. Six percent of trout treated with DHEA alone developed tumors, whereas no tumors occurred in noninitiated trout fed control or 8354-containing diets. Serum levels of androstenedione were elevated by DHEA (48-fold) or 8354 (6-fold) treatment. Serum beta-estradiol titers were increased in DHEA- but not 8354-treated trout. Vitellogenin was induced significantly by either DHEA (434-fold) or 8354 (21-fold). Peroxisomal beta-oxidation was not increased by either compound and catalase activity was decreased in DHEA-treated animals. Both steroids were potent inhibitors in vitro of trout liver glucose-6-phosphate dehydrogenase with IC50s of 24 and 0.5 microM for DHEA and 8354, respectively. This research suggests that in trout the tumor enhancing effects of DHEA may be due to its function as a sex steroid precursor and are unrelated to peroxisome proliferation. These carcinogenic properties are reduced in the analog 8354 which has been advocated as an alternative to DHEA for chemoprevention.
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PMID:Comparison of the enhancing effects of dehydroepiandrosterone with the structural analog 16 alpha-fluoro-5-androsten-17-one on aflatoxin B1 hepatocarcinogenesis in rainbow trout. 893

A randomized, single-blind, placebo-controlled study was conducted in 82 obese patients with mild to moderate essential hypertension, to determine the incidence of hyperinsulinemia, the relations between fasting insulin and dihydroepiandrosterone-sulfate (DHEA-S) levels, and the short-term effects of antihypertensives on DHEA-S and insulin serum concentrations. Increased insulin/glucose ratios (IGR) suggestive of insulin resistance were found in half of our patients. Hyperinsulinemic and normoinsulinemic obese patients with hypertension had comparable fasting glucose and DHEA-S concentrations and comparable blood pressure (BP) levels. Thus no relations were found between fasting insulin and DHEA-S levels. Fasting hyperinsulinemia was found in only half of the obese subjects with hypertension, suggesting that not all obese patients with hypertension are at the same high cardiovascular risk. Short-term treatment with captopril, prazosin, verapamil, atenolol, or hydrochlorothiazide (HCTZ) reduced BP; greater BP reduction was observed with drugs with vasodilatory effects. Captopril, prazosin, and verapamil reduced fasting insulin levels, whereas atenolol and hydrochlorothiazide did not. The former drugs reduced fasting insulin levels that were either within normal limits or in the hyperinsulinemic range. None of the drug treatments produced significant increases in serum DHEA-S concentrations, although some of them considerably reduced fasting insulin levels. No relations between insulin and DHEA-S levels were observed either at baseline or at the end of the antihypertensive treatment. The BP reduction resulting from the peripheral vasodilation may explain the insulin-reducing action of captopril, verapamil, and prazosin. These results further emphasize the large heterogeneity present in the pathophysiologic mechanisms operating in obesity and hypertension.
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PMID:Relations between fasting serum insulin, glucose, and dihydroepiandrosterone-sulfate concentrations in obese patients with hypertension: short-term effects of antihypertensive drugs. 933 14

Visceral obesity is frequently associated with muscle insulin resistance. Rats fed a high-fat diet rapidly develop obesity and insulin resistance. Dehydroepiandrosterone (DHEA) has been reported to protect against the development of obesity. This study tested the hypothesis that DHEA protects against the increase in visceral fat and the development of muscle insulin resistance induced by a high-fat diet in rats. Feeding rats a diet providing 50% of the energy as fat for 4 wk resulted in a twofold greater visceral fat mass and a 50% lower rate of maximally insulin-stimulated muscle 2-deoxyglucose (2-DG) uptake compared with controls. Rats fed the high-fat diet plus 0.3% DHEA were largely protected against the increase in visceral fat (+ 11.3 g in high fat vs. + 2.9 g in high fat plus DHEA, compared with controls) and against the decrease in insulin-stimulated muscle 2-DG uptake (0.94 +/- 0.15 mumol.ml-1.20 min-1, controls; 0.46 +/- 0.06 mumol.ml-1.20 min-1, high-fat diet; 0.78 +/- 0.07 mumol.ml-1.20 min-1, high fat + DHEA). DHEA did not affect food intake. These results show that DHEA has a protective effect against accumulation of visceral fat and development of muscle insulin resistance in rats fed a high-fat diet.
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PMID:DHEA protects against visceral obesity and muscle insulin resistance in rats fed a high-fat diet. 937 13

1. To test the hypothesis that lithium-induced body weight gain is related to an unbalance in the reproductive hormones, lithium carbonate (900 mg/day) or placebo was administered to healthy men for 1 month. 2. Body weight, skin folds and the serum levels of thyrotropic hormone, tetraiodothyroxine, prolactin, follicle-stimulating hormone, luteinizing hormone, testosterone (T5), dehydroepiandrosterone sulfate (DHEAS), estradiol (E2), cortisol, the ratios E2/T5 and T5/DHEA-S, and blood lipids were evaluated before and during treatment. 3. Body weight, skin folds, hormones and lipids serum levels were not significantly affected by the treatment with Li. These results agree with previous reports of lack of effects of 1 month-Li administration on appetite and body weight in normal male subjects (Chen et al., 1992), and question the appropriateness of studying Li-induced obesity in healthy volunteers, given the short-term administration and low doses of Li that must be used.
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PMID:Effects of lithium carbonate on reproductive hormones in healthy men: relationship with body weight regulation--a pilot study. 938 Jul 90

Long-chain polyunsaturated fatty acids (LCPUFAs), including docosahexaenoic acid ([DHA] 22:6 n-3), are important components of cell membranes. Low levels of DHA and other LCPUFAs in skeletal muscle membrane phospholipid are associated with insulin resistance and obesity in adults. These findings may be influenced by both dietary and genetic factors. This study aimed to investigate the interrelationships between the type of infant feeding, skeletal muscle phospholipid fatty acid (FA) composition, and glucoregulation in young children. Skeletal muscle biopsies and fasting blood samples were obtained from 56 normally nourished young children (35 males and 21 females) aged less than 2 years (mean +/- SE, 0.76 +/- 0.06) undergoing elective surgery. The dietary history was taken, and muscle phospholipid FA composition was analyzed. Subgroups of totally breast-fed and age-matched formula-fed infants were compared. Breast-fed infants (n = 13; age, 0.54 +/- 0.06 years) had a significantly higher percentage of DHA (3.63% +/- 0.22% v 1.84% +/- 0.11%, P < .0001) and total percentage of LCPUFAs (30.24 +/- 0.87% v 25.17% +/- 0.86, P < .0001) in muscle phospholipids compared with the formula-fed group (n = 12; age, 0.59 +/- 0.08 years). The totally breast-fed group had lower plasma glucose levels than the formula-fed group (4.7 +/- 0.2 v 5.4 +/- 0.2 mmol/L, P < .02). Consistent with these findings, further analysis of a group of 39 children who had either never or not recently been breast-fed showed significant inverse correlations between fasting plasma glucose and the percentage of both DHA (r = -.47, P < .003) and total LCPUFAs (r = -.38, P < .05). The results of this study show that (1) breast-feeding increases LCPUFA levels in skeletal muscle membrane and (2) early development of relatively higher levels of LCPUFAs in the phospholipid of skeletal muscle, influenced both by type of feeding and by genetic predisposition, is associated with lower fasting plasma glucose. Early changes in skeletal muscle membrane phospholipid FA saturation may play a role in the subsequent development of diseases associated with insulin resistance.
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PMID:The fatty acid composition of skeletal muscle membrane phospholipid: its relationship with the type of feeding and plasma glucose levels in young children. 944 Apr 87


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