Sex Hormones In Men Research Articles

Insulin resistance, body fat distribution, and sex hormones in men.

Although many studies have suggested that increased androgenicity is associated with insulin resistance and hyperinsulinemia in both pre- and postmenopausal women, relatively few data are available on this relationship in men. We examined the association of body mass index (BMI), waist-to-hip ratio (WHR), sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol with insulin concentrations and whole-body glucose disposal in 87 men from a population-based study in Kuopio, Finland. BMI was significantly correlated with fasting insulin (r = 0.46), total whole-body glucose disposal (r = -0.30), glucose oxidation (r = -0.21), and nonoxidative glucose disposal (r = -0.25). WHR also was significantly associated with fasting insulin (r = 0.61), total whole-body glucose disposal (r = -0.54), glucose oxidation (r = -0.23), and nonoxidative whole-body glucose disposal (r = -0.50). SHBG and total and free testosterone were significantly associated with insulin concentrations and total and nonoxidative glucose disposal but not with glucose oxidation. DHEA-SO4 and estradiol were not associated with insulin, glucose concentrations, or whole-body glucose disposal in univariate analysis. In multivariate analysis, total whole-body glucose disposal was associated negatively with WHR and positively associated with total testosterone and SHBG; nonoxidative whole-body glucose disposal was associated negatively with WHR and positively associated with total and free testosterone. Glucose oxidation was significantly associated only with WHR. In conclusion, higher WHR and lower testosterone were strongly associated with a decrease in total and nonoxidative whole-body glucose disposal in men.

Insulin resistance, body fat distribution, and sex hormones in men

Insulin resistance, body fat distribution, and sex hormones in men

Relation of hemostatic risk factors to other risk factors for coronary heart disease and to sex hormones in men.

The present study was carried out to explore the possible relation of plasma plasminogen activator inhibitor-1 (PAI-1), fibrinogen, and factor VII levels to other risk factors for coronary heart disease (CHD) and to serum sex hormone levels. The study group comprised 48 apparently healthy men. To avoid the confounding factor of obesity, correlations were determined in the 30 men in this group with a body mass index (BMI) < 26.4, after controlling for age. PAI-1 correlated with testosterone, estradiol/testosterone, and free testosterone/testosterone (FT/T), and fibrinogen correlated with FT/T. All three hemostatic factors correlated with glucose and with the ratio of cholesterol/high density lipoprotein cholesterol, while PAI-1 correlated with diastolic blood pressure. To test the effect of obesity, correlations were determined in the entire group of 48 men, which included 18 subjects with a BMI > 26.4. All three hemostatic factors correlated with BMI in this group after controlling for age; however, on controlling for testosterone, only PAI-1 correlated with BMI. Fibrinogen correlated with age in both groups after controlling for testosterone or BMI. These correlations support the hypothesis that PAI-1, fibrinogen, and factor VII are related to other risk factors for CHD and that an alteration in the sex hormone milieu may be the underlying factor linking them.

Endogenous sex hormones, high density lipoprotein cholesterol, and other lipoprotein fractions in men.

At least some of the large preponderance for coronary heart disease in men has been attributed to differences in lipid and lipoprotein levels; notably, high density lipoprotein cholesterol (HDL-C), a protective factor, is higher in women. The sex differences in lipid levels have been postulated to be related to differences in sex hormones. In a southern California cohort of 391 men aged 30-79 years, HDL-C levels were positively correlated and very low density lipoprotein cholesterol (VLDL-C) levels were inversely correlated with testosterone levels independently of age, body mass index, physical exercise, smoking, and alcohol intake. Mean HDL-C levels were 12% higher and VLDL-C levels were 40% lower in the highest compared with the lowest quartile of testosterone level. Low density lipoprotein cholesterol levels were positively related to estrone, estradiol, and androstenedione levels. It is premature to attribute the sex differential in lipid cardiovascular risk profiles to higher levels of testosterone per se in men, since testosterone levels are favorably associated with cardiovascular risk while estrogen levels have the converse relation in men. The differing effects and interactions of specific endogenous sex hormones in men and women require further elucidation.

Smoking and Hormone-Related Disorders

RESULTS FROM THREE PROSPECTIVE STUDIES: Smoking and oestrogen-related sites - data from American cancer studies Smoking and hormone-related disorders in the Nurses' Health Study Effects of cigarette smoking on 'hormone-related' diseases in a Southern Californian retirement community SMOKING, THE MENOPAUSE, AND THE BENIGN REPRODUCTIVE DISORDERS: Cigarette smoking and age at natural menopause Hyperemesis gravidarum, uterine fibroids, and endometriosis: effects of cigarette smoking on risk Cigarette smoking and benign breast cancer SMOKING AND OSTEOPOROSIS: Smoking and osteoporosis Cigarette smoking and skin atrophy in women - a possible connection? Smoking and prostatic hypertrophy Smoking and inflammatory bowel disease Smoking and PArkinson's disease SMOKING AND HORMONE-RELATED CANCERS: Cigarette smoking and the incidence of endometrial cancer Cigarette smoking and cancer of the breast Cigarette smoking and cancer of the large bowel MECHANISMS: HORMONAL DIFFERENCES IN SMOKERS AND NON-SMOKERS: Smoking and endogenous sex hormones in men and women Increased oxidative metabolism of oestrogens in male and female smokers The effect of smoking on hormone levels in vivo and steroid hormone biosynthesis in vitro. MECHANISMS: HORMONES OF POSSIBLE RELEVANCE TO SMOKING-RELATED DISEASES: Oestrogens and smoking-related disease: theoretical considerations Hormonal factors and cancers of the endometrium and breast MECHANISMS: THE ROLE OF NICOTINE AND OTHER AGENTS IN TOBACCO SMOKE: Influence of nicotine and other components of tobacco smoke on oestradiol metabolism Oestrogen 2-hydroxylation in rat and human liver SUMMARY AND IMPLICATIONS: Smoking and hormone-related disorders: a summary of the evidence with implications for public health policy and future research.

Effect of physical training on lipids, lipoproteins, apolipoproteins, lipases, and endogenous sex hormones in men with premature myocardial infarction

In 17 men, aged 27 to 54 years, with myocardial infarction 2 to 10 months before the current exercise study, we aimed to determine whether 3 months of exercise training, at a level designed to elevate high-density lipoprotein cholesterol (HDLC), would be associated with changes in endogenous sex steroid hormones and postheparin lipoprotein and hepatic lipases, and whether the changes in sex hormones, lipids, lipoproteins, apolipoproteins, and physical activity were interrelated. Supervised bicycle ergometry, 30 minutes, 3 days per week, eliciting 75% of maximum heart rate, produced a significant training effect, with a 26% increase in the duration of the exercise test at a standardized, submaximal workload ( P ≤ .001), and a reduction in heart rate measured at a standardized submaximal workload, P = .08. After 3 months' training, mean HDLC increased 23% (30 to 37 mg/dL), P ≤ .001, mean apo A2 increased 19% (43 to 51 mg/dL), P ≤ .001, and the ratio of total cholesterol (TC) to HDLC decreased 26% ( P ≤ .01), while estradiol (E 2) levels decreased 45% (50.1 to 27.8 pg/mL), P ≤ .0001. After 1 and 2 months' exercise, TC (12% [ P ≤ .001], 11% [ P ≤ .01]), and low-density lipoprotein cholesterol (LDLC) (13% [ P ≤ .01], 12% [ P ≤ .01]) were reduced. Hepatic lipase decreased 16% ( P ≤ .01) and 16% ( P ≤ .05) after 1 and 3 months' exercise. There were no significant changes in apo A1, lipoprotein lipase, testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), or weight. By stepwise regression analysis, after 3 months' training, 66% ( P = .0025) of the variance for the increase in HDLC from baseline to day 90 was accounted for independently by a decrease in triglyceride (F = 13.2, P = .003), by reduced heart rate on a fixed submaximal load (F = 12.7, P = .0035), and by a decrease in hepatic lipase (F = 5.5, P = .036). A modest, achievable exercise program can have significant cardiovascular benefit for men after myocardial infarction by ameliorating their hyperestrogenemia, reducing TC and LDLC, improving the TC to HDLC ratio, and elevating HDLC and apo A2. The increment in HDLC was related independently to improved capacity to sustain submaximal exercise and to exercise-induced reductions in triglyceride and postheparin hepatic lipase.

Effects of a fat-containing meal on sex hormones in men

The effect of a fat-containing meal on plasma sex steroid concentrations was investigated in normal men. After an overnight fast on two separate occasions, subjects ingested a liquid meal containing either a nonnutritive sweetener (control), or isocaloric meals of mixed calorie sources with either high-fat content or mixed carbohydrate and protein with minimal fat. The order of the meals was alternated. Blood samples were collected at 15-minute intervals and pooled each hour. Sampling began at 7:00 am and the test meal was ingested at 8:00 am. Sex steroids, including estrone, estradiol, testosterone, and dihydrotestosterone (DHT), sex hormone-binding globulin (SHBG) capacity, free testosterone concentration, and luteinizing hormone (LH) were determined by either specific radioimmunoassay or dialysis. The fat-containing meal, but not the nonnutritive or mixed carbohydrate and protein meal, resulted in a significant ( P < .01) reduction in total and free testosterone. Estrogens and luteinizing hormone were unaffected by either meal. This is the first documentation, to our knowledge, of the acute effect of a fat-containing meal on sex steroid concentrations in blood. Our observations suggest that a fat-containing meal reduces testosterone concentrations without affecting luteinizing hormone. This might indicate that fatty acids modulate testosterone production by the testes.

Abnormalities of sex hormones in men with systemic lupus erythematosus.

Sex hormone concentrations were studied in 10 men with systemic lupus erythematosus (SLE) before and after HCG stimulation and compared with those of 10 healthy volunteers. The SLE men had significantly lower testosterone/estradiol ratios (before HCG test) and significantly lower mean increases in testosterone after HCG stimulation than the normals. Our findings confirm that there are sexual hormone abnormalities in SLE and suggest that these abnormal patterns may be important in the modulation of immune responses in SLE.

Exercise training, sex hormones, and lipoprotein relationships in men.

ARTICLESExercise training, sex hormones, and lipoprotein relationships in menM. A. Frey, B. M. Doerr, L. S. Srivastava, and C. J. GlueckM. A. Frey, B. M. Doerr, L. S. Srivastava, and C. J. GlueckPublished Online:01 Mar 1983https://doi.org/10.1152/jappl.1983.54.3.757MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of physical training on lipids, lipoproteins, apolipoproteins, lipases, and endogenous sex hormones in men with premature myocardial infarctionMetabolism, Vol. 40, No. 4Levels of serum sex hormones and risk factors for coronary heart disease in exercise-trained menThe American Journal of Medicine, Vol. 79, No. 1Effects of a high-complex-carbohydrate, low-fat, low-cholesterol diet on levels of serum lipids and estradiolThe American Journal of Medicine, Vol. 78, No. 1 More from this issue > Volume 54Issue 3March 1983Pages 757-762 Copyright & PermissionsCopyright © 1983 the American Physiological Societyhttps://doi.org/10.1152/jappl.1983.54.3.757PubMed6841220History Published online 1 March 1983 Published in print 1 March 1983 Metrics