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

We have found a number of interesting hormonal abnormalities in obese men and women: 1) Obese women have normal levels of estrone, total estradiol, and total testosterone, but as a consequence of their subnormal levels of SHBG, their levels of free estradiol and free testosterone are significantly elevated. 2) Massive weight loss in obese women (to still elevated weight) results in normalization of the previously elevated free estradiol and free testosterone. 3) Obese women have normal plasma DHEA levels, but a significant, age-invariant decrease of the plasma DHEA/T ratio, which could be due to increased tissue activity of 3 beta-hydroxysteroid dehydrogenase. 4) Massive weight loss produces an age-dependent effect on DHEA levels in obese women: the levels increase to supranormal values in women around age 20, with diminishing increases at higher premenopausal ages and no increase at all at perimenopausal age. 5) Obese men have elevated levels of estrone and both free and total estradiol, and subnormal levels of free and total testosterone and of FSH; all these abnormalities are proportional to the degree of obesity. They also have relatively subnormal LH levels, i.e. normal in the face of hypotestosteronemia. The combination of these findings represents a state of mild hypogonadotropic hypogonadism (HHG), which we believe to be induced by the hyperestrogenemia. 6) Normalization of the estrogen levels of obese men, by suppression of adrenocortical secretion of aromatase substrates or by inhibition of aromatase, tends to normalize the HHG. 7) Massive weight loss in obese men normalizes their HHG without any decrease in plasma estrogen levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal abnormalities in obesity. 329 58

This study examined the prevalence of both basal and glucose-stimulated hyperinsulinemia and acanthosis nigricans (AN) as well as the relationship between insulin and androgen levels in hyperandrogenic women. Sixty-two women who had an elevation of 1 or more plasma androgen levels were studied. The results in these women, grouped for analysis on the basis of obesity and ovulatory status, were compared to those in 36 control women of similar ages and weights. The anovulatory hyperandrogenic women had the clinical and biochemical features of the polycystic ovary syndrome (PCO). Oral glucose tolerance tests were performed with measurement of glucose, insulin, sex hormone-binding globulin (SHBG), and total and non-SHBG-bound sex steroid levels. AN was present in 29% of the hyperandrogenic women, the majority of them obese. Fifty percent of obese PCO women had AN, but they did not otherwise differ from PCO women lacking this dermatological change. Only women with PCO had significant hyperinsulinemia independent of obesity, and obese PCO women with AN had the highest serum insulin levels. Plasma glucose values during the oral glucose tolerance test were significantly increased in obese PCO women independent of the presence of AN, and 20% of these women had frank impairment of glucose tolerance. Ovulatory hyperandrogenic women had normal insulin levels and glucose tolerance. Obese and nonobese women had different relationships between sex steroid and insulin levels; obese women had significant correlations between insulin and non-SHBG testosterone levels (r = 0.30; P less than 0.05), whereas nonobese women had significant correlations between insulin and FSH (r = 0.40; P less than 0.01), dehydroepiandrosterone sulfate (r = 0.33; P less than 0.05), and SHBG (r = 0.37; P less than 0.05) levels, suggesting that the mechanisms underlying the association between sex steroid and insulin levels are complex. These findings suggest that 1) only women with PCO have hyperinsulinemia independent of obesity; hyperinsulinemia is not a feature of hyperandrogenic states in general; 2) AN is a common finding in obese hyperandrogenic women, particularly those with PCO; 3) only obese PCO women are at risk for impairment of glucose tolerance, independent of the presence of AN, suggesting that the negative impact of PCO and obesity on insulin action is additive; and 4) PCO women with AN can be considered as a subgroup of PCO and do not appear to have a distinct endocrine disorder.
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PMID:Characterization of groups of hyperandrogenic women with acanthosis nigricans, impaired glucose tolerance, and/or hyperinsulinemia. 330 51

We examined sex hormone blood concentrations in a group of 33 obese non-hirsute premenopausal women with normal menses and in 14 age-matched normal-weight controls, and evaluated their relationship with anthropometric parameters, dietary habits and insulin levels. Obese women showed lower than control sex hormone-binding globulin (24.9 +/- 14.6 vs 38.6 +/- 12.5 nmol/l; p less than 0.005) and 5 alpha-dihydrotestosterone (13.7 +/- 5.4 vs 18.2 +/- 4.8 ng/dl; p less than 0.005) values. Despite their consensual behavior, the correlation coefficient between 5 alpha-dihydrotestosterone and sex hormone-binding globulin was not significant in the obese while in controls it was 0.68 (p less than 0.01). This suggests that mechanisms operating to lower the plasma levels of these compounds may be regulated differently in obesity. Body Mass Index, per cent body fat and its distribution showed a highly significant negative correlation with sex-hormone binding-globulin and 5 alpha-dihydrotestosterone values. Insulin levels did not appear to be correlated with sex hormone values. On the contrary, in the obese women we found a highly significant correlation between dietary lipids and sex-hormone-binding-globulin levels (r = -0.54; p less than 0.005) and between dietary carbohydrates and estrone values (r = 0.47; p less than 0.005); all these relationships were independent of body weight. These results confirm that in premenopausal women obesity may be characterized by detectable changes in sex steroid metabolism and suggest a possible causal role not only of the excessive quantity of metabolically active adipose tissue but also of specific dietary factors.
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PMID:Sex hormones in obese premenopausal women and their relationships to body fat mass and distribution, B cell function and diet composition. 331 65

Exogenous sex hormone use, including oral contraceptives, post-menopausal hormonal therapy and anabolic steroids, has been associated with blood pressure changes in both sexes, but little is known about the relationship between blood pressure and endogenous sex hormones. We examined this relationship in men in the Rancho Bernardo population study. Out of 1132 men aged 30-79 years, those with hypertension, categorically defined as systolic blood pressure (SBP) greater than 160 mmHg and/or diastolic blood pressure (DBP) greater than 95 mmHg had significantly lower testosterone levels than non-hypertensives. Systolic and diastolic blood pressure inversely correlated with testosterone levels (r = 0.17, P less than 0.001 for systolic; r = -0.15, P less than 0.001 for diastolic) in the whole cohort. This association was present over the whole range of blood pressures and sex hormone levels with a stepwise decrease in mean SBP and DBP per increasing quartile of testosterone. Obesity accounted for some, but not all, of this relationship, which was reduced, but still apparent after adjusting for age and body mass index. No other hormone (androstenedione, estrone, estradiol) nor sex hormone-binding globulin showed a consistent relationship with blood pressure. The clinical and physiological significance of this relationship merits further investigation.
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PMID:Blood pressure and endogenous testosterone in men: an inverse relationship. 337

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

The relationships between the hair growth in different body regions, body mass index (BMI) and age were studied in 225 women of reproductive ages referred for hirsutism. The regularity of the cycles was registered, and 109 of the patients were interviewed for their maximum weight, teenage obesity, and age of menarche. The serum androgens were measured in the follicular phase. The results indicate that facial hirsutism is associated with BMI (rho = 0.41, P less than 0.001) independently of age and the testosterone (T) to sex hormone-binding globulin (SHBG) ratio. Facial hirsutism is also correlated with age (rho = 0.37, P less than 0.001) irrespective of BMI (rho = 0.26, P less than 0.001) or the T/SHBG ratio (rho = 0.43, P less than 0.001). In contrast, the hair growth on trunk area is related to the T/SHBG ratio (rho = 0.35, P less than 0.001) but not to BMI or age when the correlations are adjusted for the grade of hyperandrogenemia. The women with severe facial hirsutism had a higher maximum weight (P less than 0.001) and more teenage obesity (P less than 0.01) than other hirsute patients. They also had a slightly earlier menarche compared with their agemates than the women with mild or absent facial hair (P less than 0.05). The data suggest differences in the regulation of hair growth between the face and trunk areas.
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PMID:Influence of body mass index and age on the grade of hair growth in hirsute women of reproductive ages. 339 96

The importance of androgenic activity in mediating the effects of obesity and body fat topography on splanchnic insulin metabolism and peripheral insulin sensitivity was studied in 19 nonhirsute premenopausal women with a wide range of ideal body weight [percent ideal body weight (% IBW), 78-202%] and body fat distribution pattern [waist to hip girth ratio (WHR), 0.67-0.91]. Turnover kinetics of peripheral plasma C-peptide and insulin were measured, and estimates of pancreatic insulin production (PIP) and the hepatic extraction fraction (HEF) were calculated. The peripheral insulin sensitivity index (M/I) was determined during an euglycemic insulin clamp study. Androgenic activity was assessed by estimating the plasma level of sex hormone-binding globulin (SHBG) and percentage of free testosterone (% FT). After iv glucose stimulation, PIP ranged from 40-254 mU/min X m2 and correlated highly with % IBW (r = 0.78; P less than 0.01). Insulin HEF ranged from 5-69% of the pancreatic production and was inversely proportional to WHR (r = -0.60; P less than 0.01). Increasing WHR also correlated with the diminution in M/I (r = -0.47; P less than 0.05), which, in turn, correlated with the decline in the HEF of insulin (r = 0.60; P less than 0.01). Since PIP, HEF, and M/I correlated with SHBG and % FT, and since the degree of androgenic activity correlated with % IBW and WHR, partial regression analysis was performed. After adjusting for the effects of SHBG and % FT, the relationship between % IBW and PIP remained unaltered, whereas the correlation between WHR and HEF or M/I and their relationship to each other were either markedly reduced or became insignificant. Thus, in premenopausal women, the increase in pancreatic insulin production with increasing weight is independent of the degree of androgenic activity. On the other hand, the decline in hepatic insulin extraction and diminution in peripheral insulin sensitivity with upper body fat localization are in part mediated by increased androgenic activity. This association may account for the pronounced hyperinsulinemia and insulin resistance characteristic of this form of obesity.
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PMID:Relationship of androgenic activity to splanchnic insulin metabolism and peripheral glucose utilization in premenopausal women. 353 81

Obesity is known to increase the risk for cancer of the reproductive tract in women. The mechanism underlying this association can be explained by increased estrogenic stimulus to estrogen-target tissues as the result of three factors. First, increased adrenal secretory activity makes more androgen precursors available for conversion to estrogen in peripheral tissues. Second, the efficiency of conversion of androstenedione (A) to estrone (E1), is elevated in obese subjects because adipose tissue is the major tissue site of conversion. Third, plasma levels of SHBG, which binds estradiol (E2), are depressed in obese subjects and greater than normal amounts of serum estradiol are therefore available to target tissues from the circulation. Recent studies have shown that the levels of estrogens and other steroid hormones in breast fluids are much higher than in serum, which may be the result of local synthesis or increased uptake from the circulation. No differences in estrogen levels of breast fluid have been found between normal women and those with breast disease. A possible explanation may be differences in the levels of estrogen antagonists, such as progesterone.
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PMID:Adipose tissue as a source of hormones. 354 69

In order to study the effect of obesity or underweight on gonadotropins and steroid hormone levels, serum concentrations of FSH, LH. Testosterone, Estradiol, Estrone, 17-OH-Progesterone and SHBG were measured by RIA in obese, underweight and control women, all menstruating in the follicular phase. Serum concentrations of all parameters measured did not differ significantly in the underweight and control groups. All obese women had higher levels of estrone than the control group, and only obese patients with a body mass index above 39 showed a lower SHBG level than that of the control group. The data suggest that the increased levels of estrone could play a role in the amenorrhea of obese women.
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PMID:[Influence of body weight on gonadotrophins and steroid hormone levels in menstruating women]. 379 88

Levels of circulating estrone (E1), estradiol (E2), androst-4-ene-3,17-dione (Adione), 3,5,3'-triiodothyronine (T3), thyroxine (T4), and sex hormone-binding globulin (SHBG) were measured in 10 obese postmenopausal patients with breast cancer and in 10 obese postmenopausal control subjects matched for age, body size, and menopausal status. T3, T4, and SHBG were also measured in 10 lean postmenopausal control subjects. In cancer patients after mastectomy, the cytosolic estrogen receptors (E2R) in tumor specimens were determined. No significant differences between the two groups of obese postmenopausal women were found for levels of all determinations carried out in serum. Comparing obese subjects (with or without breast cancer) with lean controls, circulating levels of T3 were found approximately 50% higher in the obese group. Conversely, SHBG was found around 50% of the value observed in lean controls. The changes presumably produced by obesity on serum SHBG levels appear to be reversible, tending toward normality with weight reduction. In cancer patients SHBG correlated negatively with cytosolic E2R concentrations (P less than 0.01). In conclusion, it is considered that obesity implies a double risk for breast cancer in susceptible postmenopausal women, by inducing a decrease of SHBG and a concomitant increase of the supply of "free" E2 to target tissues, in absence of cyclic endogenous progesterone.
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PMID:Decrease of circulating level of SHBG in postmenopausal obese women as a risk factor in breast cancer: reversible effect of weight loss. 394 55


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