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

Previous studies have shown that sex hormone binding globulin (SHBG) is negatively associated with insulin concentrations in premenopausal women. We determined insulin sensitivity (SI) and clearance (KI) in 8 non-obese men and 13 nonobese premenopausal women using the minimal model of Bergman and colleagues. Insulin clearance and insulin sensitivity were strongly correlated (p less than 0.05). SHBG was positively correlated with SI (i.e., individuals with high levels of SHBG had greater insulin sensitivity) in both men (r = .738, p less than 0.05) and women (r = .577, p less than 0.06). Insulin clearance was also positively correlated with SHBG in men (r = .619) and in women (r = .476) (0.05 less than p less than 0.10). Since obese subjects have both lower SHBG concentrations and decreased insulin sensitivity, we examined the effect of correcting for adiposity by partial correlation analyses. SHBG was not associated with KI after adjustment for BMI. SHBG was still positively correlated with SI in both men (r = .708) (p less than 0.06) and women (r = 0.541) (p less than 0.06), suggesting that the relationship between SHBG and insulin sensitivity is not confounded by obesity. Thus, the relationship of androgenicity with insulin sensitivity (but not insulin clearance) was independent of adiposity.
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PMID:The relationship of insulin sensitivity and metabolic clearance of insulin to adiposity and sex hormone binding globulin. 229 38

Investigation of patients presenting with hirsutism to a gynaecological endocrine clinic revealed a high incidence of anovulation, obesity and elevated androgen levels. The underlying abnormality was polycystic ovarian syndrome (PCOS) in the majority of patients. Low levels of sex hormone binding globulin were common; these increased with oestrogen treatment. Treatment with a combined oral contraceptive pill and low dose spironolactone was often effective in reducing symptoms.
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PMID:Hirsutism in a gynaecological context. 240 Mar 60

A fictitious patient with obesity, hirsutism and polycystic ovary syndrome is discussed by 3 British general practitioners to illuminate management of this type of case. The patient is 24 years old, expects to marry next year, has irregular menses averaging 6 weeks apart, and is requesting an explanation for her irregular periods as well as oral contraception. The 1st physician would exclude hypothyroidism, then evaluate polycystic ovary syndrome by assaying testosterone, LH, FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the grounds that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an essay of sex hormone binding globulin and the LH:FSH and prolactin, next find out the significance of the patient's questions in her mind and finally prescribe a triphasic pill. The 2nd doctor would withhold the pill on the ground that it might compromise future fertility if she has a primary endocrine imbalance. She would check rubella status, assay progesterone, LH, FSH, prolactin and testosterone on Day 19 of the cycle, and probably prescribe Marvelon oral contraceptives. The 3rd doctor would use a hirsutism score, investigate the polycystic ovary syndrome by ultrasound and an assay of sex hormone binding globulin and the LH:FSH ration between Days 2-6 of the cycle, and rule out congenital adrenal hyperplasia with an assay for 17-alpha-OH-progesterone. Since the patient might be anovulatory because of obesity, major long-term weight lose is a priority. Prescription of pills would depend on family history, smoking, and the degree of hirsutism and endocrine status. The most likely prescription would be a reverse sequential of cyproterone acetate 50 or 100 mcg from Days 5-15, and ethinyl estradiol 30 mcg on Days 2-25.
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PMID:Contraception and irregular menses. 259 23

A standard oral glucose tolerance test was performed in 86 healthy premenopausal obese Arab women (BMI greater than or equal to 30) Glucose, insulin and glucagon were measured at 0, 30, 60, 90 and 120 min. Sex hormone binding globulin (SHBG), plasma lipids and uric acid were also estimated. Waist-hip circumference ratio (WHR) had significant positive correlation with age, triglycerides (TG), uric acid, fasting and 120 min glucose, and 120 min insulin and significant negative correlation with SHBG. Body mass index (BMI) had significant correlation with uric acid, fasting and 120 min insulin, and significant negative correlation with high density lipoprotein cholesterol (HDL Chol). When separated in two subgroups, with WHR greater than 0.80 (41), and less than or equal to 0.80 (45 cases), plasma glucose was in the diabetic range in seven; and impaired glucose tolerance (IGT) in 11 women in the former subgroup. Only three with IGT but no diabetics, were in lower WHR subgroup. WHR in diabetics (0.93), and in IGT cases (0.90) was significantly higher than in other women (0.80). Fasting insulin was not different, but at 90 and 120 min, insulin was higher in the high WHR subgroup who had also higher fasting, 90 and 120 min glucose. Glucagon level, though slightly higher in the higher (WHR) subgroup, may indicate relative hyperglucagonaemia because of the associated significantly higher glucose. Compared with age matched non-obese controls, obese women in both subgroups had significantly higher insulin, uric acid and significantly lower HDL Chol and lower glucagon (insignificant). Obese women in the higher WHR subgroup (greater than 0.80) had also significantly higher systolic blood pressure, TG and lower SHBG.
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PMID:Pattern of obesity and insulin, glucagon, sex hormone binding globulin and lipids in obese Arab women. 269 44

An Australian study of 513 women evaluated associations between obesity and both benign and malignant breast disease, and in particular investigated the role of female sex hormones. Women who gained more than 10 kg from early womanhood had a two-fold increase in risk of developing breast cancer, whereas lean women had a greater risk of being treated for benign breast disease. Obese women with breast cancer were more likely to have Stage II tumors but there was no significant association between obesity and tumor size or estrogen and progesterone receptor status. Obesity was strongly associated with the proportions of nonprotein-bound and albumin-bound estradiol, and inversely associated with sex hormone binding globulin (SHBG) levels and the proportion of SHBG-bound estradiol. In addition, age at menarche was inversely associated, and age at menopause directly associated with recalled weight at those time periods. These data demonstrate weight gain as a risk factor for breast cancer, and suggest a possible mechanism supporting its development.
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PMID:Obesity and breast disease. The role of the female sex hormones. 275 82

Anthropometric, endocrine and metabolic variables, were examined in women with polycystic ovarian syndrome (PCO), and in normal control women. Obese women with PCO had higher plasma insulin values than non obese women with PCO, but lean body mass, glucose tolerance, plasma triglycerides and blood pressure were not different in spite of almost twice the body fat mass in the obese PCO women. However, in comparisons between non-obese PCO and control women, with equal body fat mass, the PCO women had higher blood pressure, plasma triglycerides and insulin, as well as a tendency to increased lean body mass. Both PCO groups had a high waist/hip ratio and larger abdominal fat cells than controls, indicating a preferential abdominal accumulation of adipose tissue. In comparison with abdominal adipocytes, femoral adipocytes were larger and had higher lipoprotein lipase activity in the control women, while in the PCO women these regional differences were not found. Basal and norepinephrine stimulated lipolysis were higher in the abdominal than femoral adipocytes in all groups. Substitution of the PCO women with ethinyl estradiol plus desogestrel during 6 months resulted in a regression of clinical androgenic symptoms as well as a normalization of plasma concentrations of free testosterone and sex hormone binding globulin. However, neither body composition nor metabolism were normalized. It was concluded that body fat distribution is more closely related to hypertension and metabolic derangements than total fat mass in the PCO syndrome. It is suggested that the relative paucity of femoral adipose tissue is due to a lack of specific effects of progesterone on adipocytes in this region.
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PMID:Anthropometric variables and metabolism in polycystic ovarian disease. 277 99

Most progestogens in oral contraceptives are testosterone derivatives and have androgenic side effects such as weight increase, acne and hirsutism. They pose a problem to many women just like the clinical picture of the polycystic ovary syndrome (PCO) with obesity, hirsutism, acne and amenorrhea. The aim of this study was to evaluate androgenicity of the most used progestogens with special reference to desogestrel which is a new progestogen. Radioimmunoassay was used for hormone determination while serum proteins were determined with electroimmunoassay or in some studies for sex hormone binding globulin (SHBG) with capacity assays. Serum lipids and lipoproteins were determined in serum and after ultracentrifugation in HDL, LDL and VLDL fractions. In a comparative study on levonorgestrel/ethinylestradiol (EE) (n = 10) versus desogestrel/ethinylestradiol (n = 10) the latter combination gave increases in SHBG capacity while the former did not. Similar increases in estrogen-sensitive proteins cortisol binding globulin (CBG) and ceruloplasmin indicated that the estrogenicity and "antiestrogenicity" was the same for the two combinations whereas the androgenicity of levonorgestrel was greater giving a reduction in the EE-induced increase in SHBG (SHBG is increased by estrogens and suppressed by androgens). When giving desogestrel 0.125-0.500 mg and lynestrenol 5 mg alone in daily doses to a group of regularly menstruating women (n = 8) strong suppression of SHBG was achieved while ceruloplasmin, CBG and thyroxine binding globulin (TBG) did not change. TBG is decreased and prealbumin increased by androgenic/anabolic activity but only a moderate increase in prealbumin was found during lynestrenol treatment. The changes in SHBG are probably the result of a dose-dependent receptor interaction related to 17 alpha-alkylation in 19-norsteroids. Twenty women with PCO were treated for 8 months with 0.150 mg desogestrel/0.030 mg EE. Evaluation was done before treatment and after 3 and 8 "pill" cycles regarding androgens, estradiol, SHBG, hirsutism and body weight. Spontaneous menstrual cycles were assessed after treatment. Serum lipids and lipoproteins were studied before treatment and at the end of the third "cycle". In PCO the suppression of increased total and free testosterone levels (in comparison to 22 healthy women) was evident during treatment, concordant with increases in SHBG capacity. Hirsutism was suppressed and body weight was reduced in obese women.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacodynamic studies on desogestrel administered alone and in combination with ethinylestradiol. 316 Dec 65

The very high incidence rate of breast cancer in The Netherlands, and in other Western industrialized countries, has to be explained by promoting environmental factors. The possible contributions by hormones and nutrition are reviewed. It is concluded that the promotion of breast cancer is likely to occur during breast development and several subsequent decades. A hypothesis is discussed which could explain how the affluent Western diet, a relative lack of physical activity and possibly also an overall increase of stress lead to a greater bio-availability of oestrogens at normal plasma concentrations. In this model the decrease of sex hormone binding globulin and a change of the binding equilibrium between oestrogens and plasma proteins in the presence of free fatty acids are central. Intra-abdominal fat accumulation, or frank central obesity, would favour this mechanism. Leads to further investigation and preliminary results are presented.
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PMID:Why is breast cancer so frequent in The Netherlands? 336 Jan 53

Dietary intake has been hypothesized as being associated with several hormonally related cancers including prostate, breast, ovarian, and endometrial cancer. Because diet may affect hormones directly, it is logical to examine the effects of dietary factors on hormone production and levels. Therefore, a set of 72 male MZ and 83 male DZ twin pairs was ascertained from the Utah birth certificates. A quantitative food frequency questionnaire was administered and blood samples were drawn for hormonal assays. Heritability estimates for hormonal levels were calculated indicating a range from no heritability for sex hormone binding globulin (SHBG), estrone, and testosterone glucuronide to 70% for androstanediol glucuronide and luteinizing hormone. To examine nutritional factors, the difference in hormone and SHBG levels between each MZ twin and his co-twin were correlated with the difference in nutrient intake. Weight and obesity were significantly correlated with plasma testosterone and follicle stimulating hormone. Fat intake showed a significant association with testosterone. Androstanediol glucuronide, a steroid that reflects tissue formation of dihydrotestosterone, was inversely correlated with caloric intake, theobromine and caffeine. Testosterone glucuronide exhibited significant correlations with calories and vitamin A. This study suggests that dietary intake affects plasma sex-steroid levels in men.
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PMID:The effect of nutritional factors on sex hormone levels in male twins. 336 Mar 2

A 45-year-old man, was admitted for investigation of severe sexual impairment. During 20 years of marriage, he had had no normal sexual intercourse and the couple was childless. Physical examination disclosed a severely obese man (weight 300 kg, height 1.75 m), with a relatively small and invaginated penis and small (5 ml) soft testes. Laboratory examinations disclosed the following: low serum testosterone (1 ng/ml), with a reduced response to HCG (3.8 ng/ml). Sex hormone binding globulin was at the lower limit of normal (0.38 microgram/dl), serum free testosterone was low (0.98% of total testosterone) as well as non-SHBG bound testosterone (22% of total testosterone). Daily total urinary estrogen excretion was increased (107 micrograms), the plasma estrone (78 pg/ml) and estradiol (74 pg/ml) were elevated. The gonadotropins were normal and responded adequately to LRH. Plasma growth hormone was decreased, prolactin, T4 and adrenal steroids were normal and responded normally to stimuli and inhibitors. Chromosomal constitution was 46XY. Thus, in this man the marked obesity produced a significant increase in estrogens which subsequently induced a severe decrease in testosterone and its free counterpart in excessive impairment of sexual function.
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PMID:Severe sexual impairment produced by morbid obesity. Report of a case. 339 34


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