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Population lessons from the pcos paradigm

The androgen balance is profoundly affected in the presence of metabolic disorders, particularly obesity and the metabolic syndrome (2). Androgens have an important impact on both glucose and lipid metabolism, and on fat homeostasis, therefore it is not unlikely that androgen imbalance may play a role in the pathophysiology of the metabolic syndrome. Although the few large prospective studies have not confirmed a significant association, cross-sectional studies have nonetheless provided some evidence for a linkage between low testosterone levels and CHD events, particularly in men (2). One reason for the failure to obtain conclusive information from clinical and epidemiological studies may be partly dependent on the sex-related different behavior of sex hormones in the presence of obesity. On the other hand, this hypothesis has attracted scientific concern since low testosterone in men and a condition of relative hyperandrogenism in women are associated with abdominal obesity,...

Reproductive Hormones

Obese adolescent boys appear to have an attenuated testicular response to human chorionic gonadotropin, This is probably an artifact of decreased SHBG. Indeed, Glass (65) demonstrated that despite a decrease in SHBG levels, free testosterone levels and dihydrotestosterone levels remain normal in obese subjects. Aromatization of androgens to estrogens by adipose tissue, in males, appears to be enhanced without clinical feminization (65). However, free and total testosterone levels may be diminished in morbidly obese males. This is commonly associated with decreased gonadotropin levels, suggesting some degree of hypogonadotropic hypogonadism (248). These alterations in pituitary and gonadal hormones return to normal range with weight loss (341). Indeed, since

Effects of Estrogen on Risk Factors for Diabetes

Another characteristic of postmenopausal women is androgenicity associated with low SHBG levels, which is also considered an important risk factor for insulin resistance and type 2 diabetes (120). In the Rancho Bernardo Study, SHBG was found to be inversely correlated with type 2 diabetes and impaired glucose tolerance (IGT) in postmenopausal women (130). In this regard, Andersson and associates (131) also reported that low SHBG levels were associated with type 2 diabetes in both men and women. Furthermore, they also reported that serum testosterone levels were positively correlated with the degree of insulin resistance in women. Estrogen, in contrast to androgens may increase SHBG levels. These increases in SHBG were associated with improved glucose homeostasis (132). In this context, it is also interesting that the incidence of diabetes is higher in men than in women until women reach menopause (133).

Effect of Insulin Resistance Treatment on Polycystic Ovary Syndrome Weight Loss

Weight reduction also decreases androgen levels and restores ovulation in women with PCOS (202). Most of the studies suggest a significant reduction in total testosterone and a significant increase in SHBG, positively affecting the free testosterone levels. This effect is probably as a result of the improvement in hyperinsulinemia that directly affects ovarian androgen production. Metformin (1500 mg), when administered daily for 4-8 weeks in obese women with PCOS, resulted in a decrease in insulin and free testosterone levels (210). Metformin at the above dose improved insulin sensitivity, decreased serum LH and increased serum follicle-stimulating hormone and SHBG (211). Higher plasma insulin, lower serum androstenedione and less severe menstrual abnormalities are baseline predictors of

Insulinlowering medications

Testosterone decreased and SHBG increased in a dose-related fashion with trogli-tazone treatment and was significantly different from the placebo group, and nearly all glycaemic parameters showed dose-related decreases in the treated group. Recently, Paradisi et al. (2003) demonstrated benefits of troglitazone treatment of obese women with PCOS. They have observed that after 3 months treatment with troglitazone (600mg day) there was a significant improvement in both hormonal and metabolic features (decreased free testosterone levels and insulin resistance) without significant changes in BMI. Moreover, a significant rise in endothelium-dependent vasodilatation (in response to metacholine chloride and euglycaemic hyperinsulinaemia) was documented in PCOS subjects following the treatment, with no difference from that observed in obese control women. Thus, treatment with troglitazone restored endothelial function and insulin-mediated vasodilatation in obese women with PCOS.

Other Genetic Syndromes Associated with Diabetes

Many genetic syndromes are accompanied by an increased incidence of diabetes mellitus. These include the chromosomal abnormalities of Down's syndrome, Klinefelter's syndrome, and Turner's syndrome. Wolfram's syndrome is an autosomal recessive disorder characterized by insulin-deficient diabetes and the absence of beta-cells at autopsy (87). Additional manifestations include diabetes insipidus, hypogonadism, optic atrophy, and neural deafness. These and other similar disorders are listed in Table 3.3.

Risk Factors For Obesity

Various medical genetic causes of obesity must also be considered. Endocrine conditions associated with weight gain include hypothyroidism, Cushing's syndrome, hypogonadism in the male, polycystic ovary syndrome (PCOS) in the female and growth hormone deficiency (42). Rare genetic causes of obesity include Prader-Willi syndrome, Bardet-Biedl syndrome and Cohen's syndrome. Diabetes can be an obvious consequence of the severe obesity associated with such syndromes.

Human Single Gene Mutations

Patients with Prader-Willi syndrome are characterized by hyperphagia, hypotonia, developmental delay, hypogonadism, and short stature (234). In these children, obesity may start during the first year of life and becomes prominent by the second year, which in the presence of hyperphagia can result in morbid obesity. They show extreme elevations of Ghrelin, the hunger hormone (235). It was previously suggested that a low metabolic rate caused the obesity in these children (236). However, it has been demonstrated that a lower energy requirement of these children is due to less FFM and not to an unusually low metabolic rate (237). Translocation or deletion of chromosome 15 q11-q12 uniparental maternal disomy, has been reported in about 50 of these patients (238). Lawrence-Moon-Bardet-Biedl syndrome is another dysmorphic form of obesity characterized by retinitis pigmentosa, hypogonadism, mental retardation, and polydactyly. It is inherited by an autosomal recessive gene located in...

P Michael Conn Series Editor

Male Hypogonadism Basic, Clinical, and Therapeutic Principles, edited by Stephen J. Winters, 2004 Androgens in Health and Disease, edited by Carrie J. Bagatell and William J. Bremner, 2003 Endocrine Replacement Therapy in Clinical Practice, edited by A. Wayne Meikle, 2003 Early Diagnosis of Endocrine Diseases, edited

Weight reduction by lifestyle modification

Lifestyle modification program for obese PCOS women was performed in one recent study and included a diet and exercise programme for 6 months. Obese women with PCOS were classified as responders to the intervention if they regained ovulation during the study. As a result of intervention, responders showed 11 per cent reduction in central fat, 71 per cent improvement in insulin sensitivity index, a 33 per cent fall in fasting insulin levels, and a 39 per cent reduction in LH levels, but none of these parameters changed significantly in obese PCOS who failed to restore ovulation pattern (Huber-Buchholz et al., 1999). An interventional study of 12 weeks of energy restriction and followed by 4 weeks of weight maintenance prescribing high protein or low protein diets for obese PCOS women was performed by Moran et al. (2003). They reported that pregnancies, improvements in menstrual cyclicity, lipid profile, and insulin resistance as well as decrease in weight (7.5 per cent) and abdominal...

The Metabolic Syndrome in PCOS

NCEP ATP III(+) IDF(+) group with respect to the NCEP ATP III(-) IDF(-) group. Additionally, those presenting the metabolic syndrome had significantly higher testosterone levels and selected markers of low-grade inflammation, such as white cells and fibrinogen. These data therefore confirm that the prevalence of the metabolic syndrome is higher than expected in PCOS women and that their insulin-resistant state is worsened as well as their metabolic, hormonal, and inflammatory profile.

Prenatal Androgenization and PCOS

Studies using this animal model have convincingly shown that a PCOS-like phenotype can be produced by injecting pregnant rhesus monkeys, carrying female fetuses, with 10-15 mg of testosterone propionate for 15-35 days, starting on gestational days 40-60 (early gestation) or days 100-115 (late gestation). Such treatment achieves circulating testosterone levels in female fetuses similar to those normally seen in male fetuses (31). This prenatally androgenized animal model manifests, in adult life, the reproductive and metabolic traits of human PCOS, as described below. Similar outcomes, albeit with some differences, have been reported with other animal models such as prenatally androgenized sheep and rats.

Symptomatic Treatment of Autonomic Neuropathy

Although T1DM has a high incidence rate of erectile dysfunction, it should not be taken as the causative factor without the exclusion of other possible agents. In this way, a therapy may be specifically targeted to the particular cause. The common alternative origin to erectile dysfunction is psychosomatic for which the patient should be directed to proper counseling (84). Low testosterone levels may also contribute to erectile dysfunction in which case testosterone supplementation is advised. Arteriosclerosis resulting in low genital blood flow should be directed to a vascular surgeon. The presentation of erectile dysfunction has comorbidity with other nonsymptomatic forms of DAN and atherosclerosis (85). Therefore, a thorough cardiac screening should be performed on all T1DM patients with erectile dysfunction.

Gestational Hyperandrogenism of Maternal Origin

An interesting observation made by Sir-Petermann et al. was the high prevalence of SGA births in mothers with PCOS compared with control pregnancies (12.8 vs. 2.8 ), while the prevalence of large for gestational age births were the same in both groups (69). Other studies, however, did not find a sex-specific decrease in birth weight in offsprings of PCOS women (70, 71). A study based on a random selection of pregnant women reported that endogenous maternal circulating androgen levels were negatively associated with birth size of the offspring (72). This inverse association remained unchanged after correction of several known factors associated with intrauterine growth. At gesta-tional week 17, an increase in the circulating maternal testosterone levels from the 25th to the 75th percentile corresponded to decrease in birth weight of 160 g. These findings are in accordance with animal data. For instance, in sheep, testosterone treatment of the mother during early to mid pregnancy...

Pregnancy Induced Hypertension

Hyperandrogenemia has also been examined as a possible contributor to the increased risk of PIH in PCOS patients. Laivuori et al. found mild hyperandrogenism among women with a history of preeclampsia 17 years after delivery, suggesting that the patients may have had PCOS (193). Hu et al. noted a possible role for the hyperandrogenemia of PCOS in the pathogenesis of PIH in that androgens induce production of vasoconstrictors such as endothelin and angiotensinogen (192). They found elevated total testosterone levels in PCOS patients than in controls, but no differences in DHEAS. Furthermore, studies in animal models have shown that androgens decrease the production of prostacyclin (194), which could also be a factor in the development of PIH.

Repercussions of DM in sexual life

It should be noted that DM can cause hardening and stenosis of the arteries that impede the smooth and sufficient flow of blood into the penis. At the same time, DM can cause damage in the nerves that connect the nervous system with the penis, thus leading, through this additional mechanism, to erectile dysfunction. The presence of other factors, from those already mentioned, can also aggrevate the problem (mainly smoking, hypertension, alcoholic abuse and certain categories of medicines). In rare cases the existence of hypogonadism is also a contributory factor. Overweight or obese diabetic individuals very frequently suffer from this metabolic syndrome and are characterized, among other things, by low levels of sex hormone binding globulin (SHBG). This globulin is connected in plasma with the sex hormones. Decreased levels, although affecting the total levels of testosterone, do not influence the levels of free testosterone, which are the active levels. Thus, the determination only...

Genitourinary Autonomic Neuropathy

Erectile dysfunction (ED) has many potential etiologies (including concurrent medical therapy) and so a careful initial evaluation is important in order to provide a targeted therapeutic approach. The presence of ED should alert the physician to perform a search for other modifiable cardiovascular risk factors, as cardiovascular events are reported to be increased in these subjects (155). Patients with psychogenic impotence should initially receive appropriate counseling before any other therapeutic maneuvers are undertaken (156). Testosterone supplementation should be provided if free-testosterone levels are inadequate. Atherosclerosis with resulting low penile blood flow may require a vascular surgery consultation. In males, therapy can include 50 mg or 100 mg sildenafil (157), a selective inhibitor of cyclic guanosine monophosphate-specific phosphodiesterase type 5 that is effective in about 50-60 of subjects and must not be given with organic nitrates because hypotension and fatal...

Menopausal Status and the Androgen Milieu

Similarly, the potential associations among the circulating androgen milieu total and free testosterone, dehydroepiandrosterone (DHEA), DHEA sulphate (DHEAS), and A4-androstenedione (A4A) and SF in diabetic women have been scarcely analysed, especially when studies adequately segregating both the type of diabetes and the pre- vs. postmenopausal population are considered. In contrast, several studies have analysed the concept that endogenous sex hormones may have a role in sex-dependent aetiologies of DM2, such that hyperandrogenism may increase risk in women while decreasing risk in men (55-63). In their comprehensive review, Ding et al. (56) reported that cross-sectional studies indicated that testosterone level was significantly lower in DM2 men but higher in DM2 women than in controls (p < 0.001, for sex difference). Similarly, prospective studies showed that men with higher testosterone levels had a 42 lower risk of DM2 (RR 0.58 95 CI 0.39-0.87), while there was suggestion that...

Diabetes And Erectile Dysfunction

The ability to get an adequate erection depends upon adequate blood flow to the penis and intact nerve function. Men with diabetes whose nerves to the penis are damaged and or whose blood supply to the penis is reduced may not be able to get a strong erection. Before blaming nerve damage and blood supply problems for erectile dysfunction, however, it is important to exclude other causes such as low testosterone levels, medicines (for blood pressure and depression), alcohol, and cannabis (marijuana). Psychological issues such as depression, job stress, and other relationship problems may also contribute to erectile dysfunction.

With Type Diabetes

Widom et al. (88) reported that the menstrual cycle may influence glucose metabolism in women with DM1. A subgroup of patients exhibits worsening premenstrual hyperglycaemia and a decline in insulin sensitivity during the luteal phase, and the deterioration in glucose uptake in this subgroup has been associated with a greater increment in estradiol levels from the follicular to the luteal phase. In our study, glycaemic control did not directly affect the different domains of FSFI. In fact, we did not find any significant correlations between HbA1c levels and the FSFI domains. This finding is in accord with previous reports (19) and confirmed that poor glycaemic control probably has a minor impact on SF in women. In contrast, a positive correlation was found between HbA1c values and both midfollicular-phase total testosterone and midluteal progesterone levels. This finding was contrary to those of Widom et al. (88), who reported changes in reproductive hormones not related to differing...

Androgens

Lead to increased adrenal androgen secretion. Similar altered Cortisol metabolism has been reported in obese patients (Pasquali and Vicennati, 2000). Obesity especially abdominal type of the disorder seems to amplify the degree of hyper-androgenism in PCOS. Previous studies reported that obese PCOS women have higher total and free testosterone levels compared with non-obese PCOS (Holte et al., 1994b).

Early Pregnancy Loss

Because of the contradictory results of studies examining LH hypersecretion in the pathogenesis of EPL, alternative hypotheses have been explored. Because hyperandrogenemia is common in PCOS, it has been considered as a possible cause of EPL. Aksoy et al. found elevated ratios of maternal free testosterone (expressed in pg mL) to total testosterone (expressed in ng mL) greater than 1.05 during 6-12 weeks of gestation to be predictive of subsequent miscarriage (125). In a prospective study of 50 women with a history of at least three consecutive miscarriages, Tulpalla et al. found higher levels of total and free testosterone as well as dehydroepiandrosterone sulfate (DHEA-S) among women who miscarried their next pregnancy (126). Interestingly, the presence of polycystic ovaries did not predict miscarriage. Okon et al. found higher testosterone concentrations among patients (with and without PCOS) with recurrent miscarriages than in normal fertile controls (127). There were no...

Alstrom Syndrome

This syndrome was first described in 1959, when two of Alstrom's original patients died from renal failure (86). The characteristic features of this syndrome appear to be pigmentary retinal degeneration, sensorineural hearing loss, childhood obesity, non-insulin-dependent diabetes mellitus, hyperlipidaemia, and chronic nephropathy. Features occasionally observed include acanthosis nigricans, hypogonadism, hypothyroidism, alopecia, short stature, and cardiomyopathy. A large kindred including eight affected patients has been described (87). Hyperinsulinemia and hypertriglyceridemia with normal cholesterol levels were observed in most affected individuals tested. Non-insulin-dependent diabetes and growth retardation appeared to be age-related manifestations that occurred postadolescence. Younger affected children were not overtly hyperglycaemic and were normal or above average height for age.

Bardetbiedl Syndrome

Bardet-Biedl syndrome (BBS) is an autosomal recessive condition characterized by rod-cone dystrophy (atypical retinitis pigmentosa), postaxial polydactyly, central obesity, mental retardation, hypogonadism, and renal dysfunction. Other features, not always present, include hepatic fibrosis, diabetes mellitus, reproductive abnormalities, endocrinological disturbances, short stature, developmental delay, and speech deficits. BBS is distinguished from the much rarer Laurence-Moon syndrome, in which retinal pigmentary degeneration, mental retardation, and hypogonadism occur in conjunction with progressive spastic paraparesis and distal muscle weakness, but without poly-dactyly (76). BBS was first described in 1920 (77), and the cardinal manifestations were described as retinal pigmentary dystrophy (retinitis pigmentosa), postaxial poly-

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