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Query: UMLS:C0011849 (diabetes)
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Delayed sexual maturation is still frequently seen in adolescents with type 1 diabetes. A close relationship between insulin and androgen metabolism has been found in a number of studies. Our study was designed to investigate whether or not abnormalities in androgen secretion could play a role in the onset of sexual maturation in adolescents with type 1 diabetes. We have asked whether or not there was a correlation between daily insulin dosage, duration of diabetes, metabolic control, age, pubertal stage, and body mass index (BMI) versus serum androgen concentrations. Basal total and free testosterone, dehydroepiandrosterone-sulfate (DHEA-S), dihydrotestosterone (DHT), sex hormone binding globulin (SHBG) and 3alpha-androstanediol glucuronide (3alpha diol-G) plasma concentrations were measured in 36 pubertal boys and 31 pubertal girls with type 1 diabetes and in 59 sex- and pubertal stage-matched control subjects without diabetes. Significantly higher serum total testosterone (p<0.01) and free testosterone (p<0.05) levels were found in females and males with type 1 diabetes than in controls at pubertal stage 5. DHEA-S, SHBG, DHT and 3alpha diol G concentrations in patients with diabetes were not significantly different from those in controls. There was no correlation between daily insulin requirements and serum androgen levels. These data suggest that adolescents with diabetes have similar serum levels of DHEA-S, SHBG, DHT and 3alpha diol G as healthy subjects at all stages of puberty. However, there are significant differences in serum testosterone and free testosterone levels in adolescents with diabetes when compared to healthy, sex- and pubertal stage-matched controls in late puberty. We hypothesize that the increased testosterone levels in patients with diabetes could relate to reduced fertility in females, disorders of sexual maturation and an increased risk for cardiovascular complications later in life.
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PMID:Serum androgen levels in adolescents with type 1 diabetes: relationship to pubertal stage and metabolic control. 1090 63

Obesity, the result of combined genetic and environmental factors, is in recent decades one of the most frequent diseases and is encountered mainly in Europe and North America. In women it is associated with the risk of several diseases, such as diabetes mellitus, osteoarthritis, cardiovascular diseases, sleep apnoea syndromee, breast cancer, cancer of the uterus and also with impairment of reproductive functions. Already during the last century some observations confirmed that a very low or very high body weight is more frequently associated with disorders of the menstrual cycle (MC), infertility and poor reproductive capacity. However only during the last decades the pathophysiological and molecular mechanisms of this relationship were gradually elucidated. The main factors which influences the menstrual cycle in obesity are: impaired estrogen metabolism, changes in the concentration of sex hormone binding globulin, hyperinsulinaemia, and probably also leptin levels.
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PMID:[Obesity and disorders of the menstrual cycle]. 1206 Nov 86

Many studies show that low-dose OCs have little adverse effect on carbohydrate metabolism and are safe for healthy women, women with a history of gestational diabetes, and women with insulin-dependent diabetes to use. In fact, large epidemiologic studies indicate that OCs, even the high-dose OCs (=or 50 mcg) for long periods, do not increase the risk of diabetes. There is some evidence indicating that OC use does not heighten the progression of diabetic retinopathy, nephropathy, or cardiovascular complications among women with insulin-dependent diabetes. There is no significant difference in carbohydrate metabolism among the different OC formulations. One must carefully consider the risk:benefit ratio of OC use in diabetic women since pregnancy has serious consequences for both mother and fetus. Cardiovascular complications in OC users do not originate from atherogenesis. The androgenic properties of the progestin in low-dose OCs and their effect on lipids are inconsequential for later development of coronary atherogenesis. The estrogen in OCs may protect against atherosclerosis, particularly among women at high risk of atherosclerosis. Former OC users are not at an increased risk of coronary heart disease, stroke, or other heart disease. Lipid changes in OC users tend to remain within the normal range and return to pretreatment values during the pill-free week. All OCs suppress gonadotropins and subsequent ovarian androgen production. They partially suppress androgen production by the adrenals as well. This suppression from two fronts outweighs any androgenic action of the progestin alone. Further, androgenic action probably cannot overpower the estrogen effect. The dose of levonorgestrel used in OCs is too low to express androgenic effects. Since OCs suppress androgen production, all OCs tend to improve acne. OCs reduce free testosterone and increase sex hormone binding globulin levels.
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PMID:Metabolic effects of oral contraceptives: fact vs. fiction. 1232 11

Type 1 diabetes (with predominant insulin deficiency) was until recently assumed to be the diagnosis of almost all children presenting with glucose intolerance. This requires insulin treatment via subcutaneous injections, and most patients develop microvascular and macrovascular complications in adulthood. Advances in genetics in the 1990s identified a group of genetic disorders of pancreatic beta-cell function (maturity-onset diabetes of the young) for which the outlook is better than type 1, genetic testing is available, and oral medication is the preferred treatment. In 2000, the first cases of type 2 diabetes (predominant insulin resistance) were reported in UK children, reflecting a trend seen in North America over the last 20 years. Affected children are usually overweight or obese, often female, pubertal, predominantly of ethnic minority (South Asian) origin and have a family history of type 2 diabetes. The diagnosis is aided by demonstration of insulin resistance, and may include measurement of fasting insulin and C-peptide, markers of the metabolic syndrome (fasting lipids, sex hormone binding globulin) and absence of autoantibodies against beta-cell components (e.g. glutamic acid decarboxylase). Management is aimed towards weight stabilization in the growing child, education on healthy lifestyles and the treatment of hyperglycaemia with both insulin and insulin-sensitizing agents. The underlying cause of type 2 diabetes in children is likely to be related to the epidemic of childhood obesity. There is emerging evidence of an appalling outlook for these young people in terms of miscarriages and microvascular and cardiovascular complications, which are likely to present an enormous economic and health services burden over the next 20 years.
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PMID:The emergence of type 2 diabetes in childhood. 1471 81

The aim of this study was to determine sex hormone binding globulin (SHBG) concentrations in premenopausal obese women who were otherwise healthy, and to evaluate the relationships between SHBG concentrations and features of the metabolic syndrome; 307 premenopausal women (mean age 30.9+/-10.2 years) were studied. Subjects were divided into two groups according to the BMI: Group I, women with BMI <30 kg/m2 (n=69) and Group II, women with BMI > or = 30 kg/m2 (n=238). Insulin resistance was determined according to the Homeostasis Model Assessment (HOMA) formula. Median SHBG concentration of Group I was 75.9 nmol/l. Group II was divided into two subgroups according to the median SHBG concentration of Group I; women with high SHBG (SHBG concentration > or = median level of the control group, i.e. > or = 76 nmol/l) and women with low SHBG (i.e. <76 nmol/l). The low SHBG group was significantly younger, with higher waist-to-hip ratio (WHR). Triglycerides, uric acid, insulin and HOMA values were significantly higher and HDL-cholesterol was significantly lower in the low SHBG group. Multiple regression analysis revealed that age and uric acid concentrations were significant independent predictors of SHBG concentrations in the whole group (regression summary, adjusted r2=0.1414, F=10.5627, p<0.001). It is concluded that low SHBG concentrations may indicate a severe degree of insulin resistance in premenopausal obese women.
Diabetes Nutr Metab 2004 Oct
PMID:Associations among sex hormone binding globulin concentrations and characteristics of the metabolic syndrome in obese women. 1629 51

Hirsutism in women is defined as excessive facial and/or body terminal hairs showing a masculine distribution; the condition affects approximately 7% of women of reproductive age, and chronic anovulation is a common problem for infertile couples, with a rate of 20-25%. There is a general consensus that these women should be evaluated endocrinologically, as many are found to have an androgen excess (AE) disorder. Free testosterone (FT) is the most prevalent marker in women with androgen excess, but the reference measurement procedures for FT are time-consuming and complex manual procedures that are not routinely practicable in large laboratories. Recently, models have been developed for calculating FT from total testosterone (TT), sex hormone binding globulin (SHBG), and albumin. These calculated values have been found to correlate closely with values estimated using the reference measurement procedures. This study compared measured endocrinological parameters--TT, free testosterone (aFT) by analogue ligand immunoassay method, dihydrotestosterone (DHT), dehydroepiandrosterone sulfate (DHEAS), (SHBG), And calculated parameters--calculated free testosterone (cFT), calculated bioavailable testosterone (cBT), and the free androgen index (FAI) in hirsute women and women with polycystic ovary syndrome (PCOS)--with the values in control individuals. A modified Ferriman-Gallwey score was use to describe the hirsutism pattern. No differences were observed when the measured hormone parameters were compared, while the calculated parameters were significantly increased in women in the hirsutism and PCOS groups in comparison with the values in the control group. Calculate parameters mat be more appropriate markers for assessing hyperandrogenemia in women in comparison with measured values of simple enzyme immuno-assays. These calculated values may be capable of replacing the values estimated using reference measurement procedures, so that time-consuming and complex manual procedures for measuring free testosterone with the reference methods may be dispensable in clinical practice.
Exp Clin Endocrinol Diabetes 2006 Apr
PMID:Is it necessary to measure free testosterone to assess hyperandrogenemia in women? The role of calculated free and bioavailable testosterone. 1670 50

Polycystic ovary syndrome (PCOS) is characterized by insulin resistance and consequent hyperinsulinemia. Insulin resistance also plays an important role in the metabolic syndrome (MS). We conducted a cross-sectional study to determine the prevalence of the MS in young Korean women with PCOS and whether it is associated insulin resistance. One hundred and seventeen young women with PCOS (age: 26+/-5, 16-39 years) were evaluated for the frequency of MS according to the modified Adult Treatment Panel III. Total testosterone (T), free T, androstenedione, dehydroepiandrosterone sulfate (DHEAS) and sex hormone binding globulin (SHBG) were measured, and insulin sensitivity was evaluated by euglycemic hyperinsulinemic clamp technique. The prevalence of MS in women with PCOS was 14.5%, nearly 3.5-fold higher than in age-matched women in Korean urban population (4.3%) [J.-Y. Oh, Y.-A. Sung, Y.S. Hong, E. Barrett-Conner, Prevalence and factor analysis of metabolic syndrome in an urban Korean population, Diabetes Care 27 (2004) 2027-2032]. The most frequently occurring component of MS was low HDL cholesterol (45%), and the least frequent was high fasting serum glucose level (0.9%). PCOS women with MS had significantly higher free T, and lower SHBG compared with those without MS. And women with MS showed significantly lower M-value and higher fasting/post-glucose load insulin levels. M-value was still significantly lower in women with MS even after the adjustment for BMI. MS is frequent in young Korean women with PCOS and it reflects more severe insulin resistance. These results suggest the importance of early and regular screening of metabolic disturbance in even young women with PCOS.
Diabetes Res Clin Pract 2007 Sep
PMID:The metabolic syndrome in young Korean women with polycystic ovary syndrome. 1761 Sep 84

It has been recently reported that increased serum levels of retinol binding protein 4 (RBP4), a molecule secreted by adipocytes and liver, could be an early marker of insulin resistance (IR). We determined whether serum RBP4 was increased in low birth weight (LBW)-young women as a model of early-onset IR, through a historical prospective study. The study-population included 35 LBW and 35 born at term appropriate for gestational age (term AGA) young women. Metabolic evaluations included the composite-insulin sensitivity index (composite ISI). Serum RBP4 was measured with a competitive enzyme-linked immunosorbent assay (ELISA). RBP4 levels were similar in LBW and term AGA women, while composite ISI was significantly lower in the former group. With multivariate logistic regression analysis hormonal contraception (HC) use but not birth weight, diabetes in either parents and body mass index was significantly associated with higher RBP4 levels: odds ratio = 10.6; 95% confidence interval (CI) = 2.4-76.6. In spite of higher RBP4 levels in women under HC, composite ISI was similar in women with or without HC. Women under HC also exhibited significantly higher levels of sex hormone binding globulin (SHBG), triglycerides, cholesterol, and C-reactive protein (CRP), and all of them, but not composite ISI, were significantly correlated with RBP4 levels. In conclusion, RBP4 serum level was not a marker of IR but, for the first time, it is documented a sustained increase of serum RBP4 under HC. Pathophysiological and clinical significance of this novel finding requires further investigations.
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PMID:Retinol binding protein 4, low birth weight-related insulin resistance and hormonal contraception. 1805 59

Testosterone is more than a "male sex hormone". It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.
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PMID:The many faces of testosterone. 1822 57

American men have a lifetime risk of about 18% for prostate cancer diagnosis. Large international variations in prostate cancer risks and increased risks among migrants from low- to high-risk countries indicate important roles for environmental factors. Major known risk factors include age, family history, and country/ethnicity. Type 2 diabetes appears to reduce risk, while high birth weight and adult height are linked to increased risk of aggressive prostate cancer. Limited evidence supports an association with a history of sexually transmitted infections. A previous meta-analysis of eight cohort studies indicated no associations with plasma androgen, estrogen, or sex hormone binding globulin (SHBG) levels. However, there were dose-response relationships with baseline plasma testosterone levels in two studies that adjusted for other serum hormones and obesity. Finasteride (a drug that blocks testosterone activation) reduced prostate cancer risk by 25%. Low-frequency genes linked to familial prostate cancer only explain a small fraction of all cases. Sporadic cases were linked to relatively common polymorphisms of genes involved in (1) androgen synthesis, activation, inactivation and excretion, (2) hormone and vitamin D receptors, (3) carcinogen metabolism, and (4) DNA repair. Epidemiologic evidence supports protective roles for dietary selenium, vitamin E, pulses, tomatoes/lycopene, and soy foods, and high plasma 1,25-dihydroxyvitamin D levels. There is inadequate evidence that vegetables, fruit, carotenoids, and vitamins A and C reduce risk and that animal fat, alpha-linoleic acid, meat, coffee, and tea increase risk. Two major cohort studies found dose-response relationships with dietary calcium intake. Total dietary energy intake may enhance risk. Limited evidence supports a protective role for physical activity and elevated risk for farmers and other men with occupational pesticide exposure, particularly to organochlorine compounds and phenoxy herbicides. There is inadequate evidence for a relationship with alcohol or smoking. Most known or suspected external risk factors may act through hormonal mechanisms, but our review found little supporting evidence, and substantial further research is needed.
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PMID:Role of hormonal and other factors in human prostate cancer. 1836 55


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