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)

This study examines the relationship between a series of epidemiologic parameters (age, height, body mass index (BMI), smoking, alcohol consumption, and coffee drinking) and serum concentrations of testosterone, estradiol, sex hormone-binding globulin (SHBG), and dehydroepiandrosterone sulfate (DHEAS). Among 52 healthy, elderly Greek men, we observed that serum levels of DHEAS decreased with increasing age [19% decline per 5-year increase in age, 95% CI, -2.1-(-33.5)], obesity [48% decline for BMI >30 kg/m2 compared to <27 kg/m2, CI, -15.7-(-68.7)], and current smoking [37% decline compared to nonsmokers, CI, -9.5-(-57.2)]. Estradiol concentrations increased with increasing BMI [77.1% increase for BMI >30 kg/m2 compared to <27 kg/m2, CI, -12.0-256.3], alcohol drinking [66% increase for > or = 7 glasses/week compared to <7 glasses/week, CI, 4.4-164.4], and coffee drinking [59% increase for > or = 14 cups/week compared to > or = 14 cups/ week, CI, -0.5-155.9], and decreased among current smokers [40% decline compared to nonsmokers, CI, -64.9-0.8]. SHBG was marginally positively associated with increasing age [13% increase per 5 years, CI, -0.5-29.6]. Testosterone was significantly related only to current smoking [27% decline compared to nonsmokers, CI, -45.4-(-3.1)]. These findings suggest that several variables appear to be associated with sex steroid levels and the influence of these findings on the occurrence of hormone-related conditions warrants further exploration.
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PMID:Predictors of sex hormone levels among the elderly: a study in Greece. 976 76

The purpose of this study was to investigate 24-h estradiol and leptin levels in obese and nonobese children to further understand the roles of estradiol and leptin in obesity and puberty. We measured serum estradiol, leptin, insulin, glucose, and GH levels every hour for 24 h in 18 obese (12 females and 6 males) and 30 nonobese (11 females and 19 males) prepubertal and early pubertal (stages 1-2) children. Bone age and dual energy x-ray absortiometry (DEXA) were obtained upon completion of the 24-h study. Obese children were significantly younger than nonobese children, with no difference in pubertal stage, height, or bone age between the 2 groups. Obese children had greater bone age to chronological age ratios than nonobese children, indicating a more advanced rate of bone maturation. Mean 24-h estradiol levels correlated significantly with chronological age and bone age as well as with insulin-like growth factor I, insulin-like growth factor-binding protein-3, dehydroepiandrosterone sulfate, mean 24-h GH, and lean body mass. Mean 24-h estradiol levels did not differ between obese and nonobese children [1.65+/-1.47 us. 2.75+/-3.30 pmol/L (0.45+/-0.40 vs. 0.75+/-0.90 pg/mL), respectively]. Similar mean 24-h estradiol levels in obese and nonobese children are consistent with the increased bone maturation of the obese children. Estradiol did not correlate significantly with DEXA fat mass, body mass index, or arm fat measures of adiposity. Obese children had higher 24-h mean leptin concentrations than nonobese children (28.6+/-17.4 vs. 6.8+/-7.1 ng/mL; P < 0.001). Leptin concentrations positively correlated with DEXA fat mass, body mass index, and arm fat measurement of adiposity. Girls had higher 24-h mean leptin levels than boys when controlling for adiposity. Estradiol and leptin concentrations fluctuated over a 24-h period in both groups, with all children having higher leptin concentrations at night and higher estradiol concentrations in the morning. This diurnal rhythm was of a similar pattern, but at higher levels for leptin and lower levels for estradiol in the obese children compared to nonobese children. There was no significant correlation between estradiol and leptin levels. Bone mineral density, as measured by DEXA, did not differ between obese and nonobese children. Similar bone mineral density values in obese and nonobese children are consistent with the increased bone maturation of the obese children. Bone mineral density was not correlated with estradiol or leptin level in these children. In conclusion, obese children had similar estradiol levels and equivalent bone ages at a younger chronological age than nonobese children. Leptin was higher in these obese children, but did not correlate with estradiol level or bone age. These findings suggest that the role of leptin in both obesity and pubertal development is not directly correlated with the estradiol level.
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PMID:Effect of obesity on estradiol level, and its relationship to leptin, bone maturation, and bone mineral density in children. 976 48

Excessive body weight gain is an undesirable side effect of prolonged administration of antipsychotic drugs (AP), which affects health and interferes with treatment compliance. It has been suggested that hyperprolactinemia-induced endocrine and metabolic abnormalities, particularly in the gonadal steroids, might be involved in the development of this type of weight gain. To test this hypothesis, reproductive hormones, cortisol, dehydro-epiandrosterone-sulfate (DHEA-S), thyroid hormones, and body weight gain were assessed in 18 patients (9 men, 9 women) with mental disorders receiving AP who had been medication-free for at least 3 months before the study, and in 27 placebo-treated subjects (10 men, 17 women). In women, hormones were evaluated during several phases of the menstrual cycle. A significant weight gain was observed in men but not in women. Under AP administration, women displayed significantly lower serum levels of estradiol and progesterone, whereas in men the levels of free testosterone and DHEA-S were significantly lower than in controls. Hyperprolactinemia was observed in both sexes. The levels of follicle-stimulating hormone in women and luteinizing hormone in men were significantly elevated by treatment, thus suggesting that the functioning of the hypothalamus-pituitary gonads was preserved. In men, such an endocrine profile resembles that observed in subjects with primary obesity. Women under AP administration were found to be relatively hyperandrogenic because of decreased serum estradiol levels, whereas women with primary obesity are known to display actual increased levels of androgens. These endocrine abnormalities may contribute to the excessive weight gain observed after AP treatment, and these could be the target of novel pharmacological treatments.
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PMID:Antipsychotic drugs and reproductive hormones: relationship to body weight regulation. 1008 Feb 31

Since an increase in tumor necrosis factor alpha (TNFalpha) expression has been associated with insulin resistance, this study was undertaken to determine the status of circulating TNFalpha and the relationship of TNFalpha with insulin levels, body weight, or both in women with polycystic ovary syndrome (PCOS). Fasting serum samples were analyzed in 34 subjects with PCOS, of whom 22 were obese (body mass index [BMI]>27 kg/m2), and in 40 normal control women, of whom 20 were obese. Women with PCOS exhibited a significantly (P<.02) higher mean serum TNFalpha concentration compared with the controls. The serum TNFalpha level and BMI were directly correlated in women with PCOS (r=.48, P<.005) and highly correlated in controls (r=.78, P<.001). When subjects were classified by body weight, the mean serum TNFalpha concentration was significantly (P<.001) elevated in normal-weight women with PCOS compared with normal-weight controls. On the other hand, mean serum TNFalpha concentrations in obese women with PCOS and obese controls were similar and significantly (P<.02) higher than in normal-weight women with PCOS. A direct correlation between serum fasting insulin and TNFalpha was evident in controls (r=.35, P<.03), but not in women with PCOS. However, in the subgroup of obese women with PCOS, fasting insulin directly correlated (r=.49, P<.03) with TNFalpha and the median fasting serum insulin concentration was significantly (P<.05) higher compared with the level in normal-weight women with PCOS and all controls. Fasting insulin and TNFalpha were no longer correlated in controls as a group and in obese women with PCOS when controlling for body weight. Serum TNFalpha did not correlate with luteinizing hormone (LH), testosterone (T), or dehydroepiandrosterone sulfate (DHEAS) in women with PCOS. However, serum insulin was significantly correlated (r=.49, P<.0004) with T and the BMI exhibited a trend for correlation with serum T (r=.33, P=.05) in women with PCOS. Finally, the mean serum LH concentration was significantly (P<.02) higher in normal-weight women with PCOS versus obese women with PCOS, and serum LH levels exhibited a trend for an inverse correlation with the BMI (r=.31, P=.09) in women with PCOS. We conclude that (1) serum TNFalpha is increased in normal-weight women with PCOS and is even higher in obese individuals regardless of whether they have PCOS; (2) factors other than obesity are the cause of elevated serum TNFalpha in normal-weight women with PCOS; and (3) whereas increased circulating TNFalpha may mediate insulin resistance in obesity, which may in turn promote hyperandrogenism in obese women with PCOS, it remains to be demonstrated whether this is also the case in normal-weight women with PCOS.
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PMID:Elevated serum levels of tumor necrosis factor alpha in normal-weight women with polycystic ovary syndrome. 1020 34

Insulin resistance, without frank diabetes, is associated with sudden cardiac death. We postulated that a potential mechanism for this association is autonomic dysfunction. Male Sprague-Dawley rats were randomized into one of two groups: (a) insulin resistant (IR; n = 15), or (b) control (n = 11). Animals were made insulin resistant with a fructose-rich diet, whereas control animals received standard rat chow. Four weeks after randomization, arterial pressure and baroreceptor reflex were assessed. Baroreflex sensitivity was defined as the heart-rate response to acute blood pressure changes caused by nitroprusside (0.5-18 micrograms) or phenylephrine (0.2-3 micrograms). To determine the role of vagal stimulation specifically, each animal was randomized to receive atropine sulfate (1 mg/kg) or vehicle (normal saline) before administration of phenylephrine. Mean arterial pressure and fasting insulin concentrations were increased in the insulin-resistant group, whereas there were no differences in body weight, fasting glucose concentrations, or resting heart rate. Phenylephrine increased arterial blood pressure to a maximum of 54 +/- 2 mm Hg for control and 45 +/- 6 mm Hg for IR, p = 0.7. The maximal heart-rate change response to the increased blood pressure was markedly blunted in IR as compared with control (-88 +/- 12 beats/min for IR vs. -238 +/- 18 beats/min for control; p < 0.001). Thus the baroreflex sensitivity (BRS) was threefold less in IR versus the control group (-1.8 +/- 0.2 vs. -4.6 +/- 0.7 beats/min/mm Hg; p = 0.001). Pretreatment with atropine sulfate decreased the BRS in both groups, eliminating the difference between groups (-0.96 +/- 0.5 beats/min/mm Hg for control and -0.56 +/- 0.3 beats/min/mm Hg for IR; p = 0.2). Thus atropine sulfate caused the phenylephrine-induced heart rate and arterial blood pressure response to be equal between groups. On the other hand, BRS to nitroprusside-induced blood pressure changes were similar between groups. Insulin resistance, without the confounding factors of obesity, diabetes, and significant hypertension, is associated with a large reduction in vagal activity, which occurs via attenuation in reflex activity. In contrast, the insulin-resistant syndrome does not affect baroreflex sensitivity via sympathetic reflex.
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PMID:Impaired vagal reflex activity in insulin-resistant rats. 1022 55

Serum testosterone and dehydroepiandrosterone sulfate (DHEAS) were measured in obesity and control groups using radioimmunoassay method (RIA). The sexual sign and sexual maturity were measured, too. The results showed that the contents of serum testosterone were 10.36 +/- 5.72 and (8.65 +/- 4.21) nmol/L in males of obesity and control groups respectively (P < 0.01). The levels of serum DHEAS were 8.25 +/- 6.47 and (5.63 +/- 4.98) pmol/L in femals of obesity and control groups, respectively. The length and beadth diameter of testis and length and surround of penis in males in obesity group were significantly higher than in control one (P < 0.01). The first spermatorrhea age of males in obesity group was significantly younger than that in control one (P < 0.01). Menarche age in females of obesity group and the second sexual sign development were earlier than that of control one (P < 0.01). It showed that sexual hormone, sexual development and sexual maturity were significantly higher and earlier in obesity group than those in control one.
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PMID:[The influence of obesity on sexual development in pubertal children]. 1032 97

Taste preference in obese mice was examined using genetically obese (bombesin receptor subtype-3: BRS-3 deficient) animals. Preference for either sodium saccharin (0.2%). sodium chloride (0.9%), citric acid (0.1%), or quinine sulfate (0.002%) solution was examined using a two-bottle test situation, and BRS-3 deficient mice not only showed a stronger preference for saccharin solution, but also a stronger aversive response to quinine solution, relative to wild-type littermates. Furthermore, a conditioned taste-aversion test measured the consumption of sodium saccharin (0.2%) and sodium chloride (0.9%) solutions after intraperitoneal injection of LiCl (0.3 M, 1 mg/kg), and BRS-3-deficient mice exhibited stronger aversion to both solutions than did control animals. In situ hybridization demonstrated that the BRS-3 gene is expressed in the parabrachial nucleus, the medial and central nuclei of the amygdala, and the hypothalamic nuclei such as paraventricular nucleus, all of which are known to be involved in taste perception. These results suggest that expression of the BRS-3 gene in these nuclei is important for the modulation of taste preference, as well as the development of obesity.
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PMID:Hyperresponsiveness to palatable and aversive taste stimuli in genetically obese (bombesin receptor subtype-3-deficient) mice. 1040 15

Obesity is associated to a variety of endocrine abnormalities that might lead to chronic anovulation in women. Weight loss may improve the hormonal profile and then restore ovulation in some of them. The aim of the current study was to evaluate the effect of a weight loss program on the clinical and hormonal characteristics of anovulatory obese women attending our reproductive clinic. We studied a group of 30 anovulatory obese patients between 18 and 35 years old without any thyroid disease. Before and after a weight loss of at least 5% of initial body weight we analyzed LH, FSH, estradiol, prolactine, testosterone, dehydroepiandrosterone sulfate, oral glucose tolerance test and progesterone, weight, BMI, waist/hip ratio and total body fat percentage. The mean weight loss was 9.5 +/- 4.3 kg. which represents a weight loss of 10.96% from initial body weight, with 26 patients (86.6%) resuming spontaneous ovulation. The women's mean plasma testosterone, LH, estradiol and DHEA-S decreased significantly and there was significantly increased on progesterone. At the beginning a total of 12 patients showed an impaired oral glucose tolerance test and after weight loss 9 of them improved it. The results shown in this study demonstrate that even a small weight reduction and a decrease in total body fat percentage improve the hormonal profile and restore ovulation in anovulatory obese women. Thus weight loss should be considered before starting with ovulation induction therapy.
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PMID:[Effect of weight reduction on the clinical and hormonal condition of obese anovulatory women]. 1054 39

Sex and age are the major determinants of serum levels of dehydroepiandrosterone sulfate (DHEA-S): they are about twice in men than in women and show a progressive reduction from the end of the puberty to aging in both sexes. It has been reported that DHEA-S levels are also negatively influenced by insulin. Moreover, DHEA-S levels reduction has been associated to increased risk for cardiovascular disease, which connotes hyperinsulinemic states, such as obesity. We have evaluated serum levels of DHEA-S and insulin as function of age and body mass index (BMI) in 376 adult women (age 18.1-89.6 yrs, median 42.2; BMI 15.7-57.8 kg/m2, median 32.7) by multiple regression and piecewise regression analysis. Insulin levels positively associated to BMI (p=0.000002) and DHEA-S levels negatively associated with age (p=0.000001). Considering the whole population, DHEA-S levels were related positively with BMI (p=0.0013) independently of age. DHEA-S were also directly related to insulin levels independently of age (p=0.042), but this association disappeared after correction for BMI. Piecewise regression analysis did not reveal a threshold level for the increase of BMI (p=0.0004). Interestingly, DHEA-S levels and BMI were positively associated before but not after menopause. Taking into account only obese population, (no.=143, age 18.7-67.3 yrs, mean 39.0, median 39.4) DHEA-S levels were again related negatively with age and positively with BMI, while were unrelated with waist to hip ratio (p=0.391). Our data show that increasing body mass and insulin secretion is not associated to DHEA-S reduction in women. This evidence suggests that DHEA-S is unlikely implicated in the pathogenesis of cardiovascular disease in obese women.
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PMID:Dehydroepiandrosterone sulfate levels in women. Relationships with age, body mass index and insulin levels. 1059 31

The mechanisms involved in Li-induced weight gain remain unclear. The higher frequency of obesity in women than in men under Li treatment, suggests a role for reproductive hormones. The serum levels of the following hormones were evaluated in healthy young women at diverse stages of a control menstrual cycle, and during Li carbonate (900 mg/day) or placebo administration: prolactin, luteinizing hormone, follicle-stimulating hormone, 17-1 estradiol, progesterone, thyroxine, thyrotropin, cortisol, dehidroepiandrosterone sulfate, free testosterone, leptin and an oral glucose tolerance test, in order to measure the areas under the glucose and insulin curve. The body weight was assessed the day before and the last day of treatment. The Li serum levels 15 hours after the last dose were 0.31 +/- 0.1 mEq/L. No significant changes in body weight and in the normal fluctuations of the reproductive hormones along the menstrual cycle were observed during Li administration. An increase in the serum levels of thyrotropic hormone ( p = 0.0001) was the only significant effect of Li, which may predispose to excessive weight gain after prolonged administration of the cation. The remarkable lack of effects of Li on these hormones, question the pertinence of studies conducted in healthy volunteers for the comprehension of the obesity observed in psychiatric patients who may be particularly prone to gain weight under prolonged treatment with high dose of Li.
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PMID:Endocrine effects of lithium carbonate in healthy premenopausal women: relationship with body weight regulation. 1065 79


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