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

The influences of sex hormones on the dilatation of the urinary tubules and acidophil bodies were histologically investigated in NON (Non-Obese Non-diabetic) mice. Although the dilatation of the proximal tubules and acidophil bodies in NON mice were observed only in female but not in male, a slight dilatation and a few bodies were also observed in castrated male NON mice. Moreover, in ovariectomized female NON mice the dilatation and bodies were less compared with intact female NON mice. Estradiol administration induced prominent dilatation and numerous acidophil bodies, while the administration of testosterone showed a complete preventive effect. Therefore, it is suggested that the dilatation of the tubules and the acidophil bodies can be profoundly influenced by sex hormones.
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PMID:[Effects of sex hormone on the dilatation of urinary tubule and acidophil body in NON mice]. 780 3

The first 24-cycle study of the metabolic effects of triphasic oral contraceptives (OCs) recorded significant changes in lipid values, yet none of these values moved outside the normal range. Included in the study were 69 non-smoking Canadian women 19-29 years of age with no history of obesity, diabetes, or alcohol misuse. Subjects were randomly assigned to receive either an ethinyl estradiol-norethindrone formulation (Ortho 7/7/7) or an ethinyl estradiol-levonorgestrel preparation (Triphasic). 25 controls underwent periodic blood samplings for lipid and lipoprotein levels. The only significant change recorded among controls was a 42% increase in the plasma apo B level resulting from changes in the low density lipoprotein (LDL) apo B subfraction. In the Ortho 7/7/7 and Triphasic groups, both plasma and LDL triglycerides were increased above baseline and above values for controls at the 24-month point. In Ortho 7/7/7 acceptors, LDL cholesterol increased by 28%, high density lipoprotein (HDL) decreased by 11%, and plasma cholesterol increased by 14%; other cholesterol levels decreased significantly. In the Triphasic group, HDL decreased by 8%, but no other significant changes occurred. Apo A1 increased by 15% in the Ortho 7/7/7 group, but not among Triphasic users; all apo B values increased significantly in both treatment groups. Although these changes in lipid profiles among triphasic OC users do not seem to increase the risk of cardiovascular disease, there is potential for adverse health effects when other cardiovascular risk factors, especially smoking, are present.
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PMID:A two-year clinical study of the effects of two triphasic oral contraceptives on plasma lipids. 782 Jan 62

Although many studies indicate that increased androgenicity is associated with insulin resistance and hyperinsulinemia in both premenopausal and postmenopausal women, relatively few data are available on this relationship in men. We examined the association of sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol to glucose and insulin concentrations before and during an oral glucose tolerance test in 178 men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Total and free testosterone and DHEA-SO4 were significantly inversely associated with insulin concentrations. Free testosterone and DHEA-SO4 were also significantly inversely correlated with glucose concentrations. SHBG was weakly positively associated with glucose concentrations. Estradiol was not related to glucose or insulin concentrations. After adjustment for age, obesity, and body fat distribution, insulin concentrations remained significantly inversely correlated with free testosterone (r = -.23), total testosterone (r = -.21), and DHEA-SO4 (r = -.21; all P < .01). In conclusion, we observed that increased testosterone and DHEA-SO4 are associated with lower insulin concentrations in men. This is in striking contrast to women, where increased androgenicity is associated with insulin resistance and hyperinsulinemia.
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PMID:Decreased testosterone and dehydroepiandrosterone sulfate concentrations are associated with increased insulin and glucose concentrations in nondiabetic men. 817 48

To investigate the effects on glucose and insulin metabolism of the slightly E-dominant, monophasic, low-dose oral contraceptive (OC) Diane-35, which contains 35 mcg ethinyl estradiol and 2 mg cyproterone acetate, a 17 alpha-hydroxyprogesterone derivative, the euglycemic hyperinsulinemic glucose clamp technique test was performed in 7 health young women after a one-year trial. The 7 subjects had a mean age of 22 years, a body mass index of 20.4 kg/m sq., had either never used OCs or had discontinued use at least 8 weeks before the study, were not taking medication, had no history of obesity or diabetes, and had normal glucose tolerance. The metabolic test was performed within the last 7 days before the presumed onset of menstruation during the last pretreatment cycle and within the last 5 days of OC intake during the sixth and twelfth cycle of continuous treatment with the OC. It was found that the glucose infusion rate, glucose metabolic clearance rate, and glucose infusion rate divided by plasma insulin plateau levels were not significantly affected by the OC. The metabolic clearance rate of the exogenous insulin infused during the clamp technique test was significantly increased after 6 cycles but not after 12. It was concluded that a 1-year treatment with Diane-35 does not alter peripheral (and presumable muscular) insulin sensitivity significantly, but increases insulin (presumably hepatic) clearance slightly.
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PMID:Effects of a 1-year treatment with a low-dose combined oral contraceptive containing ethinyl estradiol and cyproterone acetate on glucose and insulin metabolism. 845 99

In 22 patients with endometrial carcinoma, Stage I-III (mean age 57.8 years) with obesity, initial and reactive hyperinsulinemia (during glucose load) was revealed. Significant correlations between values of "peak" and field-square of the insulin secretion curve and cytoplasmatic receptors to Estradiol and Progesterone in the tumor were found. In a group of the patients with high values of reactive hyperinsulinemia significantly larger amounts of steroid hormone receptors in the tumor were determined as compared to the group of the patients who had low insulinemia values. On considering these data a possible conclusion was reached as to the modifying influence of hyperinsulinemia on sensitivity of endometrial carcinoma to hormone receptor synthesis in the tumor by insulin.
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PMID:Hyperinsulinemia as a factor modifying sensitivity of endometrial carcinoma to hormonal influences. 850 Apr 94

To evaluate its potential utility in counteracting neuroleptic-induced obesity, the effects of long-term administration of tamoxifen (TAM) on body weight (BW) and food intake (FI) of gonadally intact and sulpiride-treated (SUL) female rats were assessed. In addition, estradiol and prolactin serum levels were measured in rats treated with SUL. SUL plus TAM and SUL plus bromocriptine (BR). TAM, at doses of 10, 50 and 100 micrograms, significantly decreased BW gain: FI was significantly reduced at the doses of 50 and 100 micrograms. In addition, doses of TAM ranging from 5-100 micrograms completely prevented SUL-induced BW gain and hyperphagia. BR also prevented SUL effects on BW and FI. In contrast to BR, concomitant administration of TAM did not prevent SUL-induced hyperprolactinemia. Estradiol levels were not modified by SUL alone or SUL plus BR, but they were significantly increased in the animals treated with TAM plus SUL. Neuroleptic-induced obesity in female rats might be related to an alteration in gonadal steroid balance secondary to hyperprolactinemia. While BR might counteract neuroleptic-induced weight gain by preventing hyperprolactinemia, TAM might directly interact with estrogen receptors, or indirectly increase estradiol levels. The use of TAM in preventing neuroleptic-induced obesity in humans warrants further investigation.
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PMID:Tamoxifen prevents sulpiride-induced weight gain in female rats. 916 75

The role of endogenous androgens in enhancing the body's protein anabolic capacity has been controversial. To examine this question we chose to study whole-body protein and glucose kinetics in a group of 21 young, postpubertal females (16.3 +/- 0.6 yr), 8 of whom had clinical and laboratory evidence of ovarian hyperandrogenism (OH) (BMI = 37.8 +/- 1.3 kg/m2). We used L-[1-13C]leucine and [6,6,2H2]glucose tracer infusions before and after suppression of their endogenous androgens with estrogen/progesterone supplementation in the form of Triphasil for 4 weeks. Their baseline data were also compared with those of similar aged girls, 7 obese (OB) (BMI = 36.4 +/- 1.5) and 6 lean (LN) (BMI = 20.9 +/- 0.7) who were normally menstruating and had no evidence of androgen excess. Despite comparable glucose concentrations, both OH and OB groups had significant hyperinsulinemia (OH > OB), both basally and after iv glucose stimulation, as compared to LN controls (basal insulin: OH, 252 +/- 52 pmol/L; OB, 145 +/- 41; LN, 60 +/- 9, P = 0.009 OH vs. LN; peak insulin: OH, 2052 +/- 417; OB, 1109 +/- 127, LN, 480 +/- 120, P = 0.0009 OH vs. LN). The rate of appearance (Ra) of glucose, a measure of glucose production, was greater in the LN controls than in the OH or OB groups (OH, 2.0 +/- 0.1 mg/kg.fat free mass.min; OB, 1.9 +/- 0.1; LN, 3.3 +/- 0.1, P < 0.004 vs. LN). Calculated total rates of whole-body protein breakdown (leucine Ra), oxidation, and protein synthesis (nonoxidative leucine disposal) were substantially higher in the OH and OB groups as compared with LN controls (P < 0.04 vs. LN); however, when data are expressed on a per kilogram of fat free mass basis, the OH group had higher rates of proteolysis than the OB and LN, with indistinguishable rates between the latter two groups. None of the above-mentioned parameters changed after 1 month of administration of Triphasil, despite marked improvement in circulating testosterone and free testosterone concentrations after treatment (testosterone, -50%, P = 0.003; free testosterone, -70%, P = 0.02). We conclude that obesity in young postpubertal females is associated with insulin resistance for both peripheral carbohydrate and protein metabolism, and that patients with the OH syndrome have even greater insulin resistance as compared with simple obesity, regardless of treatment for the androgen excess. Carefully designed studies targeting interventions to improve both the hyperandrogenic and hyperinsulinemic state may prove useful even in the early juvenile stages of this disease.
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PMID:Ovarian hyperandrogenism is associated with insulin resistance to both peripheral carbohydrate and whole-body protein metabolism in postpubertal young females: a metabolic study. 962 16

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

The role of estradiol in mediating leptin's effects on body weight was assessed in ovariectomized (OVX) mice before and after the onset of obesity. Ovariectomy did not alter leptin levels before the onset of obesity, and estradiol adminstration (0.05-17 microgram/day for 14 days) did not significantly alter leptin levels if they were corrected for the estradiol-induced reduction in body fat. The converse was also true, in that leptin administration (0.4-140 microgram/day) did not alter estradiol levels in intact mice. Furthermore, neither estradiol reduction (via ovariectomy) nor addition (via exogenous administration) significantly altered leptin's ability to reduce fat mass. Leptin was equally effective in reducing body weight in lean or obese OVX mice and intact controls. Finally, estradiol did not change the magnitude of leptin's effect on fat mass reduction when it was given in combination with leptin to lean intact or OVX mice. Estradiol may have indirectly affected leptin efficacy, because leptin did not produce as large a change in fat mass at lower doses in lean OVX mice as it did in intact counterparts. Taken together, these data suggested that 1) estradiol does not directly regulate leptin secretion or its effects on fat mass and 2) leptin does not directly regulate estradiol secretion or its effects on fat mass. Leptin and estradiol, however, may interact in an indirect fashion to affect fat utilization.
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PMID:Does estradiol mediate leptin's effects on adiposity and body weight? 1032 91


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