Women with obesity can have increased androgen production even in the absence of PCOS, and markedly elevated androgen levels can contribute to reduced LH levels. Overall, this is in keeping with obesity being associated with increased androgen levels, which are reversed on weight loss.

This review systematically examines this core interaction mechanism: on one hand, dysfunctional adipose tissue (particularly visceral fat) exacerbates ovarian androgen overproduction by intensifying insulin resistance, inducing chronic low-grade inflammation (e.g., elevated TNF-α and IL-6), and reducing adiponectin levels. Conversely, hyperandrogenism exacerbates adipose tissue dysfunction and systemic insulin resistance by altering body fat distribution (central obesity), suppressing lipogenesis, impairing lipolysis, and disrupting adipokine secretion.

Circulating androgen levels are highly correlated with the degree of insulin resistance and risk of metabolic syndrome observed in women with PCOS, often independently of obesity. Hyperinsulinemia can in turn increase androgen generation from both ovarian theca cells and within metabolic tissues themselves, such as adipose tissue, leading to a vicious cycle of metabolic and steroid hormone dysfunction.

In women, obesity and metabolic syndrome is associated with increases in androgen levels. Obese women have elevated levels of testosterone although the levels are only increased 2–3 fold and thus are still significantly lower than in men. Obesity in women, including women with polycystic ovary syndrome and those who are postmenopausal, is associated with increases in serum testosterone.

In a nationally representative sample of US girls, obesity is associated with elevated free testosterone, suggesting an important relationship between obesity and peripubertal hyperandrogenemia. Previous clinical studies have suggested that peripubertal obesity is associated with elevated total and free testosterone levels, including in pre- and early pubertal girls.

This review suggests that severe adiposity causes “metabolic/functionally atypical” PCOS by enhancing ovarian steroidogenesis through hyperinsulinism and adipose- and gut-dependent proinflammatory adipokines in genetically predisposed individuals, plus amplifying the ability of adipose tissue to generate testosterone and adrenal-derived 11β-hydroxytestosterone from circulating precursors. The hyperandrogenic environment created within adipose tissue by adiposity-dependent and independent insulin-resistant hyperinsulinism, intra-adipose steroidogenesis, and PCOS-related hyperandrogenemia also appears to restrict the capacity of subcutaneous adipose to safely store fat, predisposing to ectopic fat deposition and lipotoxicity with weight gain.

We found elevated androgen levels in the obese cohort compared to the lean cohort... Serum androgen levels were significantly higher in obese women than in lean.

Blood production rates of testosterone, dihydrotestosterone (DHT), and 3α-androstanediol (3α-diol) were found to be approximately 2-fold elevated in morbidly obese, nonhirsute, normally menstruating women. Thus, obesity is a state of increased androgen production and accelerated clearance.

The heavier women had lower serum dehydroepiandrosterone (DHEA), dihydrotestosterone (DHT), and sex hormone-binding globulin (SHBG) (P < 0.05 for all) compared to their leaner co-twins with no differences in serum testosterone or androstenedione levels. Serum DHEA correlated inversely with %body fat (r = -0.905, P = 0.002), and DHT positively with SHBG (r = 0.842, P = 0.002). Serum DHEA levels were best predicted by %body fat, and serum DHT by SHBG.

Women with a surplus of visceral adipose tissue also have increased ovarian androgen production, likely caused by elevated insulin levels that often occur with obesity. A possible mechanism leading to increased androgen levels comes through the binding of insulin to its receptors on theca cells, inducing an increase in LH activity at the ovarian level, which, in turn, stimulates androgen production and secretion.

Strong evidence indicates that insulin resistance, with the associated compensatory hyperinsulinemia, may play a major pathogenic role in this syndrome. It enhances androgen secretion from both the ovaries and the adrenals and reduces SHBG synthesis in the liver, thus increasing free androgen levels. However, the association between body fat and hyperandrogenism seems to be to a large extent explained by insulin resistance.

Obese women, particularly those with the abdominal phenotype, tend to develop a condition of functional hyperandrogenism.

Second, hyperinsulinemia suppresses hepatic production of sex hormone-binding globulin (SHBG) and IGF-binding proteins, thereby increasing circulating free androgen and IGF-1 levels that further stimulate ovarian androgen synthesis. Third, and notably, elevated expression and activity of AKR1C3 in adipose tissue of PCOS patients—this enzyme converts androstenedione to testosterone—creates a local insulin-androgen activation feedback loop that amplifies androgen production within adipose tissue itself.

Regardless of hormone therapy use, higher current BMI (≥30 vs. <25 kg/m^2) was associated with higher serum concentrations of DHEAS, 5α-reduced glucuronide metabolites, and DHEAS:DHEA ratio. Waist–hip ratio was positively associated with adrenal androgens and 5α-reduced glucuronide metabolites in obese women only (BMI ≥30 kg/m^2). These findings suggest that obesity and central fat distribution are associated with alterations in androgen metabolism among postmenopausal women.

Obesity, oligomenorrhea, and hirsutism are frequently associated with high plasma androgen levels and/or low testosterone-binding globulin (TEBG) levels. A striking new finding was that subjects with the combination of obesity and oligomenorrhea had elevated plasma total and free androgens and depressed TEBG even in the absence of hirsutism.

A significant negative correlation between SHBG and body mass index (BMI) was observed in PCOS, IH, and C women. In obese women—whether PCOS, IH, or C—free testosterone (fT) levels were significantly higher and, conversely, SHBG levels were lower than in non-obese women. Upper-body obesity was associated with lower SHBG and higher fT levels than lower-body obesity. In conclusion, obesity, particularly upper-body obesity, is associated with a reduction in SHBG and an increase in fT in both nonhirsute and hirsute women.

Levels of SHBG and albumin were inversely related to body mass index. The percentage and concentration of non-SHBG-bound testosterone and the free androgen index were directly related to body mass index. The distribution of total testosterone into SHBG-bound and non-SHBG-bound fractions is associated with body mass index, not with PCOS.

Androgen excess is often associated with obesity states, at any age of life, because of changes in the pattern of secretion or metabolism of androgens and in their actions at the level of target tissues, particularly the adipose tissue.

The free active testosterone concentrations in plasma are very much influenced by SHBG concentrations because only 1–2% of testosterone in the circulation is free (unbound) and active; 65% is bound to SHBG and the rest is bound to albumin. Therefore, women with low SHBG can have normal total testosterone levels but elevated bioavailable and free testosterone levels. Interestingly, the meta-analysis found, in good and fair quality studies, that women with PCOS have had obesity related metabolic abnormalities associated with significantly lower SHBG levels but not with indices of hyperandrogenism, which highlights the possibility that decreased SHBG occurs prior to increased androgens in PCOS.

The steroidogenic enzyme activity of adipocytes appears to be relevant in the development of hyperandrogenism in PCOS, particularly because weak androgens such as androstenedione are rapidly taken up, sequestered from circulation by mature adipocytes, and converted into strong androgens. Adipocytes produce potent androgens, and androgens modulate adipocyte proliferation, hypertrophy, macrophage invasion, and overproduction of various adipocytokines that stimulate steroidogenic cell secretion.

Excess androgens can be induced by insulin resistance and hyperinsulinemia, as they cause a reduction in sex hormone binding globulin levels, which lead to a subsequent increase in free androgens and unfavourable metabolic profiles. Obesity and insulin resistance may also amplify androgen production by ovarian theca cells and adrenal glands, contributing to hyperandrogenemia in women with PCOS.

Weight gain and obesity in women with PCOS, through their effects on insulin resistance, drive enhanced steroidogenesis and hyperandrogenism. This provides an explanation for the close association between body weight and severity of the hyperandrogenic features of PCOS. Furthermore, 5-alpha reductase activity correlated positively with increasing adiposity in both PCOS and control women.

There is growing evidence that obesity in women lead to a more severe form of hyperandrogenism and other endocrine abnormalities. In hirsute women with BMI >= 25 kg/m2 measured total testosterone was significantly higher, SHBG was significantly lower and the calculated androgen parameter... were significantly higher compared to women with BMI < 25 kg/m2.

Our findings highlight that obesity exhibited a significant correlation with lower levels of sex hormone binding globulin (SHBG) and elevated levels of free androgen index (FAI), fasting insulin, and HOMA-IR in PCOS patients diagnosed with insulin resistance (IR). Our study revealed that in patients with PCOS who also had IR, obesity exhibited a correlation with lower levels of SHBG and higher levels of FAI, but did not show a significant association with lipid levels or sex hormone levels. In summary, our study established a strong association between obesity and reduced SHBG levels or increased FAI levels among PCOS patients with IR, thus indicating the potential utility of SHBG or FAI as a biomarker for initial identification and prognosis of IR in obese PCOS patients.

Obesity and body fat distribution have independent roles in the development of hyperandrogenism in PCOS. Abdominal body fat distribution in obese women with PCOS amplifies the degree of hyperandrogenism... Both loss of body weight and/or the reduction of the degree of hyperinsulinemia... reduce blood androgen levels.

Studies of patients with PCOS showed increased local androgen production by AKR1C3 and lipid accumulation in the adipose tissue leading to lipotoxicity, insulin resistance, and compensatory hyperinsulinemia. Collectively, these findings demonstrated that hyperandrogenism attenuates adipokine levels with insulin-sensitizing properties that may have detrimental consequences on insulin sensitivity in women with PCOS.

Androgen metabolism is accelerated in obesity. Evidence of alterations in adrenocortical steroidogenesis has been presented, suggesting a selective obesity-related enhancement in adrenal androgen secretion. These reproductive endocrinologic alterations in obese women may contribute to androgen excess and menstrual disturbances.

These findings define an intra-adipose mechanism of androgen activation that contributes to adipose remodeling and a systemic lipotoxic metabolome, with intra-adipose androgens driving lipid accumulation and insulin resistance in PCOS. Adipose androgen generation mediated by AKR1C3 was shown to be increased in PCOS, linking local androgen activation in fat with systemic metabolic dysfunction.

Androgen excess may also contribute to adipocyte insulin resistance by suppressing production of the insulin-sensitizing adipokine adiponectin. Thus, although the mechanism remains unclear, testosterone in conjunction with a high-calorie diet seems to promote visceral fat accumulation and insulin resistance in females by a combination of inhibiting lipolysis and promoting lipogenesis.

When looking at cross-sectional studies, elevated weight, BMI, or adiposity is generally associated with lower SHBG levels. This relation is particularly evident in studies of women, where higher levels of adiposity are associated with decreased SHBG concentrations. Because SHBG strongly influences the proportion of free (bioavailable) testosterone, lower SHBG with higher adiposity can result in increased free androgen levels even if total testosterone is unchanged.

Obese women, especially those with upper body obesity, have insulin resistance and hyperinsulinaemia, hyperandrogenaemia, increased peripheral aromatization of androgens to oestrogens, altered gonadotrophin secretion, decreased sex hormone binding globulin, and altered neuroregulation of the hypothalamic-pituitary-gonadal axis.

A negative correlation was observed between SHBG and actual body weight (ABW), both in controls (P < 0.05) and hirsute patients (P < 0.01). Inverse correlations between SHBG and ABW, % ideal body weight (% IBW), and ABW/H2 were observed in group 2 but not in group 3. We conclude that a negative relationship exists between SHBG and the body size in nonobese women and that in hirsute patients, obesity leads to a further lowering of SHBG through mechanism(s) probably independent of androgens.

Although many factors are involved, resistance to insulin and enhanced level of androgen are considered the major causes of PCOS. Obesity further worsens insulin resistance and hyperinsulinemia, which in turn stimulates androgen production from the ovaries and adrenals and decreases SHBG, thereby increasing free androgen levels.

The 11-oxygenated androgens are considered to be higher in patients with obesity and PCOS than in healthy counterparts without obesity. They are positively correlated with insulin resistance.

Specifically, cross-sectional studies have reported that lower androgen levels in men and higher androgen levels in women are associated with greater visceral fat area measured by computed tomography. Previous cross-sectional studies have also suggested that visceral adiposity is associated with greater androgenicity in women, i.e. higher calculated bioavailable testosterone and lower SHBG concentrations. Among overweight adults with impaired glucose tolerance, reductions in either visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were associated with increased total testosterone in men and higher SHBG in men and women.

In women, reduced levels of sex hormone-binding globulin (SHBG) associated with abdominal obesity may suggest that elevated free androgens contribute to increased visceral fat accumulation. Abdominal obesity has been linked to lower plasma testosterone levels in both cross-sectional and longitudinal studies. Thus, in women, altered SHBG and androgen status appear to be related to body fat distribution, particularly visceral fat.

This is because low concentrations of SHBG, for example in insulin resistance or obesity, can affect total testosterone values. Obesity is listed as a diagnosis of exclusion; hyperandrogenism is usually present, menstrual problems are uncommon.

Serum total testosterone levels did not correlate directly with body fat distribution in either early or late postmenopausal groups. The free testosterone (FT) in early postmenopausal women and the DHEA-S levels in late postmenopausal women correlated positively with the trunk/leg fat ratio and the proportion of android fat, whereas they correlated negatively with the proportion of gynoid fat. These results suggested that SHBG was not an independent factor associated with abdominal fat accumulation and the FT was independent from SHBG and total testosterone to predict abdominal fat accumulation.

Aim of the present study is to evaluate hormones like free testosterone and sex hormone binding globulin in obese women with polycystic ovary syndrome (PCOS). This study showed that biological hormones such as testosterone were significantly higher that reflects low sex hormone binding globulin (SHBG) in obese women with PCOS compared to the age-matched controls having normal body weight and ovulatory menstruation. It has been found that women with polycystic ovary syndrome (PCOS) are mainly overweight or obese showing the evidence that increase in body weight increases hyperandrogenic state in women.