Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: A common endocrinopathy with distinct pathophysiologic features

Barbieri, Robert L.; Ryan, Kenneth J.

doi:10.1016/0002-9378(83)90091-1

Cited by 285 publications

(152 citation statements)

References 54 publications

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“…43 ' 4445 Increased percent free testosterone and total testosterone are associated with insulin resistance independently of obesity in premenopausal women. 44 On the other hand, hyperinsulinemia can cause increased androgen production by the ovary, 46 and insulin has recently been shown to suppress the production of SHBG in a human hepatoma cell line. 47 In this report, we have proposed that increased androgenicity (as measured by decreased SHBG) is associated with increased insulin and triglyceride concentrations and decreased HDL cholesterol, but we cannot exclude the possibility that the decreased SHBG and HDL cholesterol are both consequences of hyperinsulinemia.…”

Section: Discussionmentioning

confidence: 99%

Association of decreased sex hormone binding globulin and cardiovascular risk factors.

et al. 1989

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Sex hormones play a major role in determining the risk of cardiovascular disease. While earlier studies have shown that reduced sex hormone binding globulin (SHBG) Is associated with increased glucose and Insulin concentrations in premenopausal women, few data exist on the relationship of SHBG to other cardiovascular risk factors in women. We hypothesized that decreased SHBG would be associated with an atherogenlc pattern of cardiovascular risk factors. We measured total testosterone, total estradlol and SHBG, llplds and lipoproteins, glucose and insulin, and systolic and dlastolic blood pressure In 96 premenopausal women. Although total testosterone and total estradiol were not related to cardiovascular risk factors, SHBG was negatively associated with trlglycerlde concentration (r=-0.37) and positively associated with high density llpoproteln cholesterol (HDLC) (r=0.42). After adjustment for overall adiposity (body mass index) and upper body adiposity (as measured by the ratio of waist-to-hlp circumferences), SHBG was still positively related to HDLC, but not to trlglycerlde. Adjustment for Insulin abolished the relationship between SHBG and triglyceride levels, but did not alter the relationship between SHBG and HDLC. Sex hormones were not related to either systolic or dlastolic blood pressure. (Arteriosclerosis 9:136-143, January/February 1989) S ex hormones play a major role in determining the risk of cardiovascular disease. Indirect evidence for this concept is provided by the higher triglyceride and low density lipoprotein cholesterol (LDLC) and lower high density lipoprotein cholesterol (HDLC) levels in men than in women.1 More direct evidence for the role of sex hormones as determinants of cardiovascular risk factors is provided by studies showing that exogenous androgen administration increases LDLC and decreases HDLC. 23 Conversely, administration of estrogens to postmenopausal women with familial hypercholesterolemia is associated with decreased LDLC and increased HDLC. 4 Sex hormone binding globulin (SHBG) may also be an important predictor of lipids and lipoproteins, since it is the major determinant of the ratio of free to bound plasma testosterone and other androgens. 5 Although decreased SHBG and increased percent free testosterone have been associated with increased glycemia and insulinemia in premenopausal women, 67 few data exist on the relationship of endogenous sex hormones and SHBG to lipids and lipoproteins. Studies to date suggest that SHBG is positively associated with HDLC in both premenopausal 8 and postmenopausal 9 women.

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Section: Discussionmentioning

confidence: 99%

Association of decreased sex hormone binding globulin and cardiovascular risk factors.

et al. 1989

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“…In these instances, a glucose tolerance test may be necessary to reveal the underlying abnormality of insulin resistance. 2 To evaluate the possibility of hyperandrogenism, total testosterone should be measured on two to three occasions. Levels of 17␣-hydroxyprogesterone, dehydroepiandrosterone sulfate (DHEAS) and morning cortisol after a low dose of dexamethasone should be determined, as should levels of luteinizing and follicle-stimulating hormones, depending on physical findings, history and concern about an ovarian or adrenal abnormality ( Table 2).…”

Section: Laboratory Studiesmentioning

confidence: 99%

“…Suppression of gonadotropins with estrogen-progesterone oral contraceptives has also been shown to help by reducing the production of ovarian androgen. 2 Contraceptives containing newer progestins, such as desogestrel (Desogen) and norgestimate (Ortho-Cyclen), appear to have fewer androgenic side effects and may be safer to use in persons with abnormal lipid levels or hirsutism.…”

Section: Treatmentmentioning

confidence: 99%

Clinical Presentation and Differential Diagnosis

Scott

2013

Myelodysplastic Syndromes

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“…The factors which promote epidermal proliferation have not been completely elucidated, but the main hypothesis is based upon stimulation through growth factors such as melanocyte-stimulant hormone, growth hormone, adrenocorticotrophic hormone and insulin, among others 10 . In the human ovary, current evidence, both in vitro and in vivo allow us to state that insulin connects to specific receptors or to IGF-1 Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The presence of raised serum insulin levels in patients with PCOS and hyperandrogenism was initially elucidated by Burghen et al 8 and Taylor et al 9 . Nevertheless it was Barbieri and Ryan 10 , who, in 1983, described a group of patients with PCOS, HA, peripheral insulin resistance (IR) and acanthosis nigricans, naming it as HAIR-AN syndrome. According to the authors, the insulin resistance raised circulating insulin levels, which, in turn, excess would act in the ovaries and epidermis.…”

Section: Introductionmentioning

confidence: 99%

Ovarian activity before and after gonadal suppression by GnRH-a in patients with polycystic ovary syndrome, hyperandrogenism, hyperinsulinism and acanthosis nigricans

Motta¹,

Baracat²,

Haidar³

et al. 1998

Rev. Assoc. Med. Bras.

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SUMMARY -OBJECTIVE.To investigate the ovarian activity before and after gonadal suppression with GnRH-analog in patients with PCO, hyperandrogenism, hyperinsulinism and acanthosis nigricans. Design: Controlled clinical study. Setting: Tertiary academic medical center. Patients: Six patients with clinical findings of PCO, hirsutism and acanthosis nigricans.INTERVENTIONS. Morning blood samples in the follicular phase to determine the steroid levels, glucose and insulin curve, comparing to a control group. Administration for 2 consecutive months of a GnRH-analog, comparing, in the study group, the free testosterone levels before and after ovarian suppression.MAIN OUTCOME MEASURE. Determination of insulin levels in PCO, hirsutism and acanthotic patients and the free-testosterone levels before and after gonadal suppression.RESULTS. Insulin levels were significantly higher in the study group when compared to normal women during the glycemic test. We also found a significant decrease in the free-testosterone levels after 2 months of gonadal suppression with GnRH-analog when compared to the initial time.CONCLUSIONS. Patients with PCO, hirsutism and acanthosis nigricans present high levels of insulin, suggesting an ovarian hyperesponsiveness, which is not sustained when gonadotrophic blockage was achieved.

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Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: A common endocrinopathy with distinct pathophysiologic features

Cited by 285 publications

References 54 publications

Association of decreased sex hormone binding globulin and cardiovascular risk factors.

Association of decreased sex hormone binding globulin and cardiovascular risk factors.

Clinical Presentation and Differential Diagnosis

Ovarian activity before and after gonadal suppression by GnRH-a in patients with polycystic ovary syndrome, hyperandrogenism, hyperinsulinism and acanthosis nigricans

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