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)

The patient was a 16-month-old girl, born by mature natural delivery and weighing 3,320 g. Hirsutism was noted on birth. Development of pubic hair and hypertrophy of the labia minora were noted after 8 months. At the time of admission, the height was 80 cm and body weight 14.5 kg. Systemic obesity, facial acne, systemic hirsutism, low pitched voice and hypertrophied clitoris were observed. Androstenedione, dehydroepiandrosterone-sulfate and cortisol showed high levels in the blood, and the urinary 17-KS was obviously high, along with an increase in urinary 17-OHCS. The subject did not respond to either the dexamethasone inhibition test or ACTH load test. The abdominal CT revealed a tumor in the front upper position of the left kidney, and adrenal scintigraphy disclosed an obvious accumulation image in the adrenal gland on the left side. Based on the diagnosis of a left adrenal tumor, left adrenalectomy was performed. The tumor measured 5.0 x 4.5 x 3.7 cm, and weighed 57 g. Histopathologically it was diagnosed as adrenocortical adenoma. The infantile virilizing adrenocortical tumor is reported together with some discussion of the literature.
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PMID:[A case of infantile virilizing adrenocortical tumor]. 261 Jan 80

Obese (n = 8) and nonobese (n = 6) adult rhesus monkeys (Macaca mulatta) were assessed in terms of body size and distribution of body fat, glucose tolerance, and serum lipid, insulin, and androgen levels. The weights of the obese monkeys were more than 2 SD above the mean for their sex, while the nonobese monkeys averaged less than 0.25 SD from the mean. Obese males and females had excess body fat located predominantly in the abdominal region; abdominal circumference was highly correlated with total body fat, as estimated by the isotope dilution method (r = 0.98; P less than 0.001). Obese monkeys of both sexes had fasting hyperinsulinemia, greater insulin response to iv glucose administration, and marginally impaired glucose tolerance. Obese males had delayed maximal insulin response to glucose administration. Fasting serum triglycerides also were elevated in the obese monkeys (0.95 +/- 0.08 vs. 0.47 +/- 0.05 mmol/L; P less than 0.001). Obese males had lower serum dihydrotestosterone levels than nonobese males (3.1 +/- 0.7 vs. 5.6 +/- 0.4 nmol/L; P less than 0.01). Nonobese females had approximately 2-fold higher serum dehydroepiandrosterone sulfate levels than the other groups. We conclude that obese male and female rhesus monkeys have patterns of fat distribution and glucoregulatory abnormalities similar to those of humans with upper body obesity. The contribution of differences in androgen metabolism to the development of obesity and its complications in rhesus monkeys remain to be defined.
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PMID:Obesity in male and female rhesus monkeys: fat distribution, glucoregulation, and serum androgen levels. 266 27

This disposition of acetaminophen was examined in an overfed rat model of human obesity following iv administration of a subtoxic 303 +/- 5 mg/kg dose based upon ideal body weight. Weanling Sprague-Dawley rats were maintained on a nutritionally complete semisynthetic diet containing 60% vegetable shortening and were compared to animals given a standard laboratory diet over the same 22-week period. At the time of study obese rats outweighed controls by 42% (637 +/- 32 g vs. 450 +/- 7 g, respectively). The absolute clearance of acetaminophen from plasma increased by 27% in obese rats. Higher partial formation clearance to acetaminophen glucuronide and sulfate conjugates accounted for most of this increase. Clearance by sulfhydryl conjugation was also substantially increased (56%), indicating that metabolism via toxic oxidation also occurred at a greater rate in obese animals. Absolute renal clearance of the glucuronide and sulfate conjugates but not acetaminophen increased with obesity, whereas parent volume of distribution remained unchanged. Some rats raised on the energy-dense diet remained lean and were examined separately as a dietary control group. Acetaminophen disposition in these animals was indistinguishable from pellet-fed controls, suggesting that acetaminophen elimination changes in overweight animals resulted from obesity itself and not from the obesity inducing energy-dense diet. Although animals placed on the energy-dense diet ate fewer grams of food per day, their caloric intake was similar to that of pellet-fed animals when adjusted for differences in body weight and caloric content of the diets.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An overfed rat model that reproduces acetaminophen disposition in obese humans. 287 25

Analysis of the clinical findings and growth in 20 boys with isolated gonadotropin deficiency revealed a heterogeneous group of physical abnormalities. Ten of these patients were hyposmic or anosmic (Kallmann syndrome). Abnormalities found in our patients included undescended testes, gynecomastia, and ocular or skeletal anomalies. Regardless of the presence of hyposmia, patients without testicular enlargement (less than 2 cm3), had serum luteinizing hormone (LH) responses to luteinizing hormone-releasing factor (LRF) that were the same as in prepubertal boys. By contrast, five boys with testicular enlargement (greater than 2 cm3), some of whom had hyposmia, had a greater serum LH response to LRF than did prepubertal boys. Adrenarche was moderately delayed; although all boys initially had normal serum levels of dehydroepiandrosterone-sulfate, four boys eventually developed elevated serum levels. Bone ages were delayed compared with chronologic age in boys who had the condition after 15 years of age. The rate of linear growth was normal, and final adult heights were normal with testosterone therapy, although linear growth continued longer in these boys than in boys with normal pubertal progression. Although none of the patients was obese at the time of diagnosis, three patients developed obesity after initiation of testosterone therapy.
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PMID:Isolated gonadotropin deficiency in boys: clinical characteristics and growth. 288 18

In order to verify the relationship between insulin resistance and hyperandrogenism in Polycystic ovary disease (PCOD), circulating levels of insulin in response to oral glucose tolerance test (OGTT) were assessed in 23 PCOD patients and 10 matched control subjects without obesity, acanthosis nigricans and impaired glucose tolerance. In PCOD patients serum total testosterone (T), dehydroepiandrosterone sulfate (DHEA-S), LH and LH/FSH ratio were significantly higher than in control subjects; whereas urinary 17-ketosteroids (17-KS) and glycemic response to OGTT were not different. PCOD patients were clearly hyperinsulinemic before and during OGTT compared to the control group: mean +/- SD basal insulin (Io) (23.4 +/- 10.3 vs 11.3 +/- 4.6 microU/ml, p less than 0.001) and the sums of insulin levels (sigma I) during OGTT (341.4 +/- 148.9 vs 162.2 +/- 56 microU/ml, p less than 0.001). In the two groups serum T, but not DHEA-S, LH, urinary 17-KS and the degree of obesity, was strongly associated with Io (r = 0.458, p less than 0.01) and sigma I (r = 0.419, p less than 0.02), as well as with insulin resistance as assessed by basal (r = 0.425, p less than 0.02) and postglucose challenge (r = 0.384, p less than 0.05) insulin to glucose ratio. These results confirm that the hyperinsulinism and insulin resistance in PCOD is not related to obesity and suggest that the hyperandrogenism may be partially responsible of the observed imbalance in glucose-insulin homeostasis.
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PMID:Insulin resistance and secretion in polycystic ovarian disease. 293 64

The ovarian ultrasonic appearance in 20 patients with polycystic ovarian disease was studied and correlated to the clinical, hormonal, and laparoscopic findings. Ultrasound studies showed that both ovaries were enlarged in 15 patients (15.46 +/- 2.5 cm3). Maximum ovarian surface area was 9.75 +/- 3.38 cm2. Three ultrasonic patterns were detected: (1) isoechoic, with no discernible cysts (four patients); (2) hypoechoic, with multiple small cysts of less than 1 cm (11 patients); (3) hypoechoic, with single cyst of greater than 1 cm (five patients). Ultrasonic estimation of ovarian size was superior to clinical assessment and equal to that of laparoscopic examination. Subtle differences existed between the ultrasonic appearance of the ovaries in hyperprolactinemic subgroups of polycystic ovarian disease compared to normoprolactinemic ones. However, no significant relationship was found between the ovarian size and any of the hormones studied. Obesity, amenorrhea, hirsutism, hyperprolactinemia, and elevated testosterone and dehydroepiandrosterone sulfate levels were more common in the group with enlarged ovaries, whereas oligomenorrhea, elevated luteinizing hormone/follicle-stimulating hormone ratio, and elevated androstenedione and estrone levels occurred more frequently in the group with normal-sized ovaries. The value of ultrasound studies in the management of polycystic ovarian disease is emphasized.
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PMID:Correlation of the ultrasonic appearance of the ovaries in polycystic ovarian disease and the clinical, hormonal, and laparoscopic findings. 293 74

It has been postulated that dehydroepiandrosterone (DHEA) and its sulfate ester, dehydroepiandrosterone sulfate (DHEAS), the major secretory products of the human adrenal gland, may be discriminators of life expectancy and aging. We examined the relation of base-line circulating DHEAS levels to subsequent 12-year mortality from any cause, from cardiovascular disease, and from ischemic heart disease in a population-based cohort of 242 men aged 50 to 79 years at the start of the study. Mean DHEAS levels decreased with age and were also significantly lower in men with a history of heart disease than in those without such a history. In men with no history of heart disease at base line, the age-adjusted relative risk associated with a DHEAS level below 140 micrograms per deciliter was 1.5 (P not significant) for death from any causes, 3.3 (P less than 0.05) for death from cardiovascular disease, and 3.2 (P less than 0.05) for death from ischemic heart disease. In multivariate analyses, an increase in DHEAS level of 100 micrograms per deciliter was associated with a 36 percent reduction in mortality from any causes (P less than 0.05) and a 48 percent reduction in mortality from cardiovascular disease (P less than 0.05), after adjustment for age, systolic blood pressure, serum cholesterol level, obesity, fasting plasma glucose level, cigarette smoking status, and personal history of heart disease. Our conclusions are limited by the single determination of DHEAS levels, but the data suggest that the DHEAS concentration is independently and inversely related to death from any cause and death from cardiovascular disease in men over age 50.
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PMID:A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease. 294 52

The steroid prehormone, dehydroepiandrosterone (DHEA) has potent antihyperglycemic effects when fed in the diet of genetically diabetic C57BL/KsJ-db/db mice. The purpose of this investigation was to analyze changes in sex steroid levels in serum of mice fed DHEA, and to compare the antihyperglycemic potencies of the various metabolites in order to clarify the mechanism of DHEA action. Steroid radioimmunoassays showed that dietary DHEA entered the blood in high concentrations and was actively metabolized to both androgens (testosterone, T; dihydrotestosterone, DHT) and estrogens (estrone, E1; 17 beta-estradiol, E2). This metabolism did not require intact adrenal glands or gonads. In C57BL/KsJ normal (+/+) males, conversion of DHEA to androgens was the prominent feature; in db/db males, DHEA feeding not only increased serum T and DHT, but also serum E1 and E2 levels. The db/db mice had increased amounts of adipose tissue that sequestered more intravenously injected 3H-E2; this additional body fat could account for increased aromatization of DHEA-derived estrogen precursors. Comparisons of the relative antihyperglycemic potencies of androgenic and estrogenic steroid metabolites of DHEA in db/db mice showed that the estrogens and metabolites with estrogenic properties (androstenediol) or those convertible to estrogens (DHEA sulfate) were the most potent. Although 17 beta-E2 was effective by injection or per os, DHEA was effective only when administered per os, implicating alimentary tract conversion of DHEA to more biologically active reactants. Based on the pivotal position of DHEA as a prehormone for androgens, estrogens, and etiocholanolones, an explanation of the seemingly paradoxical effects exerted by this compound in blocking autoimmune disease, hyperglycemia, obesity, and neoplasia was proposed.
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PMID:Androgenic and estrogenic metabolites in serum of mice fed dehydroepiandrosterone: relationship to antihyperglycemic effects. 295 67

Heritability of the variation of the plasma concentrations of total and unbound cortisol, cortisol binding globulin (CBG), and dehydroepiandrosterone sulfate (DHEA-S) was investigated in 20 monozygotic (MZ) and 20 dizygotic (DZ) male twin pairs. Three plasma samples collected between 8 AM and 9:30 AM were pooled for the assays. Heritability was calculated from the intraclass correlation [2(rMZ - rDZ)]. The mean age, total and unbound cortisol, CBG, and DHEA-S were not significantly different between the MZ and DZ groups of twins. The heritability index for variability of the plasma content of steroids was 45.4% (p less than .05) for total cortisol, 50.6% (P less than .05) for unbound plasma cortisol, 57.8% (P less than .05) for DHEA-S, and 32.4% (P greater than .05) for CBG. The data were analyzed by factor analysis, and heritability estimates were corrected for factors including age, smoking, drinking, exercise, and degree of obesity. These factors did not account for the variation in hormone values in twin pairs. Factor analysis of the three quantitative measurements, cortisol, percent free cortisol, and DHEA-S, provides no evidence for shared factors. The correlation coefficients between age and CBG and total and unbound plasma cortisol concentrations were insignificant. The correlation coefficient between total plasma cortisol levels and CBG was 0.57, which indicates that CBG accounts for 32% of the variation of plasma cortisol concentrations. The results suggest that genetic factors have a decided influence on the variation of the concentration of cortisol of DHEA-S in normal adult men.
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PMID:Heritability of variation of plasma cortisol levels. 296 19

The glucagon receptor and the adenylyl cyclase system of human liver membranes were studied in six non-obese and six obese subjects who had elevated insulin and plasma glucagon levels. Analysis of specific glucagon binding by the method of Scatchard demonstrated a linear (monocomponent) plot with a dissociation constant of 2-3 nM, and the binding at low hormone concentrations was sensitive to guanosine triphosphate (GTP). The molecular weight of the glucagon receptor was 63,000 D as determined by an affinity labeling procedure and sodium dodecyl sulfate gel electrophoresis. Affinity labeling of this structure was specific for glucagon and inhibited by GTP. Glucagon stimulated the production of cyclic adenosine monophosphate (cAMP) by human membranes with half-maximal activation elicited by 6 nM hormone. The human cyclase system required GTP to facilitate an optimal glucagon response. NaF (10 mM) also activated the cyclase system and produced the same magnitude of response as maximum glucagon activation. A comparison of the liver adenylyl cyclase system of non-obese and obese subjects was made using glucagon (5 nM and 1 microM) and NaF (10 mM). No significant differences in cAMP production were noted between the two groups, regardless of the agent used to activate the enzyme. These findings agree with the glucagon binding studies that showed similar amounts of binding activity in the membranes from the two groups. Also, there was no influence of either age or sex of the subjects on the adenylyl cyclase response. In conclusion, human liver membranes contain a glucagon receptor and an adenylyl cyclase system that correspond closely to the well-studied system in animal liver. This system in human obesity is not altered by the approximately twofold elevation in plasma glucagon that occurs in this metabolic disorder.
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PMID:Glucagon receptor of human liver. Studies of its molecular weight and binding properties, and its ability to activate hepatic adenylyl cyclase of non-obese and obese subjects. 298 13


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