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

In some countries, the incidence of obesity doubles every 10 years. For the obstetrician-gynecologist, there are many different situations where the patient's excess body weight calls for an adapted diagnostic and therapeutic approach. Obesity does not in itself appear to be a factor lowering fertility. However obesity-induced hormone disorders could contribute, in certain cases, to biological imbalance and thus favor the development of ovulation dysfunction. Pregnancy in obese women should be managed as a high risk pregnancy. The incidence of gestational diabetes and hypertension is increased. Macrosomatia is frequent. There is a 2- to 3-fold increase in the rate of cesarean sections with more complications. Fetal morbidity does not appear to be changed when maternal weight gain is limited. With obesity, there is an increased risk for breast and endometrial cancer due, for most authors, to elevated levels of circulating estrogens resulting from aromatization of male sex steroids in adipose tissue and decreased levels of sex hormone-binding globulin. Anesthesia and surgery in obese patients can be problematic and special care must be taken to prevent further morbidity. Laparoscopic surgery is possible under certain conditions, although its role remains to be determined. Prescription of hormone replacement must take into consideration several parameters which determine its usefulness and surveillance. Obesity is not a contraindication for hormone replacement therapy but is frequently a non-indication.
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PMID:Obesity in obstetrics and gynaecology. 957 82

This study examined the relationship of hepatic and peripheral insulin sensitivity and beta-cell secretory function with serum sex hormone-binding globulin (SHBG) in men and women with Type 2 diabetes mellitus (DM). Fasting insulin, glucose and SHBG were measured in 58 Type 2 diabetic patients of both sexes (36 men) who were on diet treatment only and terms for insulin sensitivity and beta-cell secretion obtained by modelling. There was no significant difference in SHBG between men and women despite similar degree of obesity. SHBG was positively correlated (r = 0.41, p < 0.01) to hepatic insulin sensitivity derived from mathematical modelling of fasting glucose and insulin data using the homeostasis assessment model (HOMA). This relationship was independent of gender (men, r = 0.48, p < 0.01; women, r = 0.45, p < 0.05). Fasting insulin correlated negatively with SHBG in men (r = -0.34, p < 0.05). There were also significant negative correlations between SHBG and either plasma glucose (r = -0.29, p < 0.05) or body mass index (r = -0.34, p < 0.05). SHBG did not correlate with HOMA-modelled beta-cell function. In a multiple regression analysis, SHBG was independently correlated only with insulin sensitivity (p < 0.05). Further studies in 15 of the diabetic patients (11 men), showed a significant positive correlation (r = 0.52, p < 0.05) between SHBG and peripheral insulin sensitivity derived by continuous infusion of glucose with model assessment (CIGMA) but not between SHBG and CIGMA-modelled beta-cell function. These results indicate that both hepatic and peripheral insulin sensitivity are similarly related to serum SHBG in Type 2 diabetes of both sexes. The sex-difference in SHBG was abolished in the patients.
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PMID:Serum sex-hormone-binding globulin is related to hepatic and peripheral insulin sensitivity but not to beta-cell function in men and women with Type 2 diabetes mellitus. 963 21

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

Hyperinsulinemia is a risk factor for cardiovascular disease, and is linked with non-insulin-dependent diabetes mellitus (NIDDM), hyperlipidemia, obesity, and hypertension. Sex hormones also play a role in the metabolic alterations associated with the risk for cardiovascular disease. A reduction in sex hormone-binding globulin (SHBG) may be predictive of future NIDDM particularly in women. The postmenopausal decline in estrogen is also associated with an increase in risk factor expression in women. Since African Americans experience a greater prevalence of NIDDM, obesity, and hypertension, conditions associated with hyperinsulinemia, the purpose of this study was to determine if alterations in sex hormone levels are associated with the plasma insulin concentration in young adult African Americans, and to determine if there are sex differences in the effect of insulin on lipids and sex hormones. In a sample of 221 nondiabetic African American men (n = 105) and women (n = 116) with a mean age of 31 years, we examined the relationship of the plasma insulin concentration with the body mass index (BMI), blood pressure, plasma lipids, and sex hormones, including free testosterone, estradiol, and SHBG. Plasma insulin increased with the BMI and other measures of adiposity (P<.001) in men and women. Significant correlations of insulin with plasma lipids were also present in both sexes. There was a significant inverse correlation of insulin with SHBG in both men (r = .28, P = .007) and women (r = .27, P = .02). There was a significant direct correlation of insulin with free testosterone in women (r = .032, P<.001). Stepwise multiple regression analyses with insulin as the dependent variable detected the BMI, triglyceride, and apolipoprotein A1 as significant contributors to the plasma insulin concentration in men. In women, the multiple regression model detected percent body fat, low-density lipoprotein (LDL) cholesterol, and free testosterone as significant contributors to plasma insulin. These data on young African Americans demonstrate a significant relationship between hyperinsulinemia and obesity, atherogenic lipid status, and lower SHBG. In the premenopausal women, the lower SHBG is linked with higher free testosterone, favoring a condition of relative androgen excess.
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PMID:Hyperinsulinism and sex hormones in young adult African Americans. 992 Jan 53

Low levels of sex hormone-binding globulin (SHBG) are considered to be an indirect index of hyperinsulinemia, predicting the later onset of diabetes mellitus type 2. In the insulin resistance state and in the presence of an increased pancreatic beta-cell demand (e.g. obesity) both absolute and relative increases in proinsulin secretion occur. In the present study we investigated the correlation between SHBG and pancreatic beta-cell secretion in men with different body compositions. Eighteen young men (30.0 +/- 2.4 years) with normal glucose tolerance and body mass indexes (BMI) ranging from 22.6 to 43.2 kg/m2 were submitted to an oral glucose tolerance test (75 g) and baseline and 120-min blood samples were used to determine insulin, proinsulin and C-peptide by specific immunoassays. Baseline SHBG values were significantly correlated with baseline insulin (r = -0.58, P < 0.05), proinsulin (r = -0.47, P < 0.05), C-peptide (r = -0.55, P < 0.05) and also with proinsulin at 120 min after glucose load (r = -0.58, P < 0.05). Stepwise regression analysis revealed that proinsulin values at 120 min were the strongest predictor of SHBG (r = -0.58, P < 0.05). When subjects were divided into obese (BMI > 28 kg/m2, N = 8) and nonobese (BMI < or = 25 kg/m2, N = 10) groups, significantly lower levels of SHBG were found in the obese subjects. The obese group had significantly higher baseline proinsulin, C-peptide and 120-min proinsulin and insulin levels. For the first time using a specific assay for insulin determination, a strong inverse correlation between insulinemia and SHBG levels was confirmed. The finding of a strong negative correlation between SHBG levels and pancreatic beta-cell secretion, mainly for the 120-min post-glucose load proinsulin levels, reinforces the concept that low SHBG levels are a suitable marker of increased pancreatic beta-cell demand.
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PMID:Low levels of sex hormone-binding globulin and hyperproinsulinemia as markers of increased pancreatic beta-cell demand in men. 995 50

To assess the differential impact of the insulin secretory pattern and obesity on the endocrinometabolic features of the polycystic ovary syndrome (PCOS), we studied 110 PCOS women. Patients underwent a gonadotropin-releasing hormone (GnRH) test, an oral glucose tolerance test (OGTT), and basal evaluation of hormonal and biochemical parameters. Basal androgens and lipids, basal and stimulated gonadotropins, insulin, and glucose levels were measured. Patients were classified into four groups according to the body mass index (BMI) and insulin secretion: normoinsulinemic-lean ([NL] n = 24), normoinsulinemic obese ([NO] n = 24), hyperinsulinemic lean ([HL] n = 17), hyperinsulinemic obese ([HO] n = 45). HL patients showed a higher luteinizing hormone (LH) area under curve (AUC) after GnRH stimulus compared with NL patients (HL v NL, 4,285 +/- 348 v 3,377 +/- 314 IU/L x 120 min, P < .05), whereas we failed to find a statistically significant difference in a similar comparison among obese subjects (HO v NO, 3,606 +/- 302 v 3,129 +/- 602 IU/L x 120 min). A trend toward increased plasma testosterone and decreased sex hormone-binding globulin (SHBG) was found in relation to hyperinsulinemia and obesity, thus resulting in a higher free androgen index (FAI) in groups HL and NO versus NL (HL, 5.54 +/- 0.51; NO, 5.64 +/- 0.49; NL, 4.13 +/- 0.33; P < .05 and P < .01, respectively). The presence of both exaggerated insulin secretion and obesity resulted in a synergistic additive effect on the FAI in the HO group (6.81 +/- 0.34). Concerning the lipoprotein lipid profile, the NL group showed lower plasma triglyceride levels compared with the other three groups, whereas no significant differences were found for nonesterified fatty acid (NEFA) concentrations. Higher low-density lipoprotein cholesterol (LDL-C) and very-low-density lipoprotein cholesterol (VLDL-C) and lower high-density lipoprotein cholesterol (HDL-C) levels were found in the obese groups compared with the lean counterparts, whereas the same parameters did not significantly differ in a comparison between normoinsulinemic and hyperinsulinemic groups. In conclusion, our data suggest an important role of hyperinsulinemia in the LH response to a GnRH stimulus and an independent and synergistic additive effect of obesity and hyperinsulinemia on the FAI in PCOS.
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PMID:Impact of insulin and body mass index on metabolic and endocrine variables in polycystic ovary syndrome. 1002 76

Weight reduction and exercise have been shown to help with menstrual disturbance and infertility in obese women with polycystic ovary syndrome. We studied the relationship between insulin sensitivity and ovulation patterns in 18 infertile anovulatory obese polycystic ovary syndrome (PCOS) women (NO) with normal glucose tolerance, aged between 22-39 yr with a body mass index of 27-45 kg/m2, before and after a 6-month diet and exercise program. This program promotes healthy lifestyle factors, but does not lead to rapid weight loss. The anthropometric, metabolic, and endocrine factors of these subjects were compared to those of 10 age- and weight-matched PCOS women with regular monthly ovulation (RO). Before lifestyle modification, the anovulatory subjects had greater central obesity than regular ovulators, as assessed by percent central fat (NO, 45.7 +/- 0.8%; RO, 42.2 +/- 1.6%; P < 0.05), higher glucose increment after glucose challenge (NO, 10.1 +/- 1.0 mmol/L; RO, 6.4 +/- 1.1 mmol/L; P < 0.02), lower insulin sensitivity index (NO, 1.2 +/- 0.2; RO, 2.8 +/- 0.6 micromol/kg x min/pmol/L; P < 0.005), higher plasma LH (NO, 8.9 +/- 0.9; RO, 4.6 +/- 0.9 IU/L; P < 0.005), and lower plasma sex hormone-binding globulin (NO, 18.0 +/- 2.5; RO, 27.8 +/- 5.7 nmol/L; P < 0.05]. Anovulatory subjects were classified as responders (R) to the intervention if they regained ovulation during the study. As a result of intervention, R showed an 11% reduction in central fat, a 71% improvement in insulin sensitivity index, a 33% fall in fasting insulin levels, and a 39% reduction in LH levels. None of these parameters changed significantly in nonresponders (NR). At the end of the study, R had lower fasting insulin (R, 13.6 +/- 1.7; NR, 23.0 +/- 3.5 mU/L) and LH levels (R, 5.0 +/- 1.7; NR, 7.4 +/- 1.4 IU/L), but similar androgen levels compared to NR. We conclude that lifestyle modification without rapid weight loss leads to a reduction of central fat and improved insulin sensitivity, which restores ovulation in overweight infertile women with PCOS. Lifestyle modification is the best initial management for obese women seeking to improve their reproductive function.
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PMID:Restoration of reproductive potential by lifestyle modification in obese polycystic ovary syndrome: role of insulin sensitivity and luteinizing hormone. 1019 97

Many adolescents present with hirsutism and irregular menses. The challenge for the clinician is to distinguish physiologic anovulatory cycles from true menstrual disorders such as PCOS, and to differentiate PCOS from other causes of hyperandrogenism in hirsute adolescents. Common clinical features seen in adolescents with PCOS include hirsutism, acne, menstrual irregularity, and obesity. Biochemical abnormalities include hyperandrogenism, acyclic estrogen production, LH hypersecretion, decreased levels of SHBG, and hyperinsulinemia. Management strategies for a patient with PCOS include treatment of features which may cause distress to the adolescent, such as hirsutism, acne, and irregular menses, and prevention of long-term sequelae. Oral contraceptive pills, antiandrogens, and cosmetic treatments are used to treat hirsutism, acne, and menstrual irregularity. Oral contraceptive pills or medroxyprogesterone acetate are given to prevent endometrial hyperplasia and carcinoma. Counseling about weight loss and nutrition are essential, as weight loss may improve signs of hyperandrogenism and menstrual irregularity and may prevent NIDDM and cardiovascular disease. Insulin-sensitizing agents show promise in terms of decreasing hyperandrogenism, restoring ovulatory cycles, treating infertility, and preventing long-term sequelae. Finally, it is important to recognize that adolescents with PCOS may experience psychological distress because of the clinical manifestations of hyperandrogenism or when confronted with the information that they have a chronic illness. Psychological support should be available for these young women. Future research is likely to further elucidate the pathophysiology of PCOS, identify candidate genes, and clarify which adolescents are at risk for long-term sequelae. Prospective studies are needed to identify which therapies could potentially reduce the risk of infertility, diabetes, cardiovascular disease, and endometrial carcinoma in young women with PCOS.
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PMID:Polycystic ovary syndrome. 1037 Jul 13

The fundamental clinical features of PCOS include hirsutism and menstrual irregularities from the time of menarche. Obesity is present in approximately 50% of these patients, some of whom also carry a diagnosis of NIDDM. The biochemical abnormalities associated with the clinical picture include LH hypersecretion, hyperandrogenism, acyclic estrogen production, subnormal SHBG levels, and hyperinsulinemia. Hirsutism usually progresses slowly in patients with PCOS; however, the clinical presentation can resemble virilizing tumors, late-onset CAH, or Cushing syndrome. Virilization or rapidly progressive hirsutism requires immediate investigation to rule out a virilizing tumor. Goals of therapy for teenage patients include decreasing levels of bioavailable androgen, blockade of androgen action at target tissues, stabilization of the endometrium, and reduction of insulin resistance. Although the original description of PCOS by Stein and Leventhal was published in 1935, the cause of PCOS remains unknown. This reason, coupled with the fact that PCOS-related insulin resistance is an important cause of NIDDM in women, has caused this disorder to become one of interest and active investigation. Future research will likely be able to delineate mechanisms behind the defects of carbohydrate metabolism and ascertain large multigeneration kindreds for linkage analyses to identify affected genes. Future studies are also likely to confirm whether young women with PCOS are at increased risk for cardiovascular disease and other long-term health complications. As new pathophysiologic mechanisms are identified, the promise of new therapies arises, including treatments that could potentially reduce the long-term incidence of adverse health consequences.
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PMID:Menstrual disorders in adolescents. Excess androgens and the polycystic ovary syndrome. 1038 5

Leptin circulates in plasma at concentrations that parallel the amount of fat reserves. In obese males, androgen levels decline in proportion to the degree of obesity. Recently, we have shown that in rodent Leydig cells leptin inhibits hCG-stimulated testosterone (T) production via a functional leptin receptor isoform; others have found that leptin inhibits basal and hCG-induced T secretion by testis from adult rats. In this study, we further investigated the relationship linking leptin and androgens in men. Basal and hCG-stimulated leptin and sex hormone levels were studied in a large group of men ranging from normal weight to very obese (body mass index, 21.8-55.7). Initial cross-sectional studies showed that circulating leptin and fat mass (FM) were inversely related with total and free T (r = -0.51 and r = -0.38, P < 0.01 and P < 0.05, respectively). Multiple regression analysis indicated that the correlation between leptin or FM and T was not lost after controlling for SHBG and/or LH and/or estradiol (E2) levels and that leptin was the best hormonal predictor of the lower androgen levels in obesity. Dynamic studies showed that in obese men the area under the curve of T and free T to LH/hCG stimulation (5000 IU i.m.) was 30-40% lower than in controls and inversely correlated with leptin levels (r = -0.45 and r = -0.40, P < 0.01 and P < 0.05, respectively). Also, LH/hCG-stimulation caused higher increases in 17-OH-progesterone to T ratio in obese men than in controls, whereas no differences were observed between groups either in stimulated E2 levels or in the E2/T ratio. In all subjects, the percentage increases from baseline in the 17-OH-progesterone to T ratio were directly correlated with leptin levels or FM (r = 0.40 and r = 0.45, P < 0.01), but not with E2 or other hormonal variables. In conclusion, our studies, together with previous in vitro findings, indicate that excess of circulating leptin may be an important contributor to the development of reduced androgens in male obesity.
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PMID:Leptin and androgens in male obesity: evidence for leptin contribution to reduced androgen levels. 1052 13


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