Glucose action and adrenocortical biosynthesis in women with polycystic ovary syndrome

Farah-Eways, Lisa; Reyna, Rosario; Knochenhauer, Eric S.; Bartolucci, Alfred A.; Azziz, Ricardo

doi:10.1016/j.fertnstert.2003.05.008

Cited by 40 publications

(22 citation statements)

References 40 publications

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“…The increase seen in DHEA was larger than the increase in androstenodione. Similarly, Farah-Eways et al (52) reported that, after ACTH stimulation, serum DHEA increased by 222% and androstenodione increased by 31% in patients with PCOS, whereas DHEA increased by 266% and androstenodione increased by 68% in healthy control women. Although testosterone is the main excessive androgen in PCOS, depending on patients' ethnicity, 20 -30% of patients with PCOS have high serum concentrations of DHEAS (25,53).…”

Section: Discussionmentioning

confidence: 83%

Relation of nutrients and hormones in polycystic ovary syndrome

Kasim-Karakas

Cunningham

Tsodikov

2007

The American Journal of Clinical Nutrition

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Background: Insulin resistance, infertility, and hirsutism, common characteristics of polycystic ovary syndrome (PCOS), improve with even modest weight loss. Optimal dietary treatment for PCOS is not known. Objective: We compared the effects of acute protein administration with those of glucose challenges on hormones related to obesity and insulin resistance (ie, cortisol and insulin), hirsutism [ie, dehydroepiandosterone (DHEA) and androstenedione], and hunger (ie, ghrelin). Design: Patients with PCOS (n ҃ 28; aged 26 Ȁ 2 y) were tested with a 5-h oral-glucose-tolerance test (OGTT) and a euvolemic, euenergetic protein challenge. Results: Glucose ingestion caused larger fluctuations in blood glucose and more hyperinsulinemia than did protein (P 0.01, overall treatment-by-time interaction). During the protein challenge, cortisol and DHEA declined over 5 h. During OGTT, cortisol and DHEA increased after the third hour and began to show significant divergence from protein from the fourth hour (P ͨ 0.01). During OGTT, 18 patients who had a blood glucose nadir of 69 mg/dL had elevated cortisol (baseline: 10.4 Ȁ 0.4; nadir: 5.9 Ȁ 0.1; peak: 12.7 Ȁ 0.9 g/dL) and DHEA (baseline: 15.6 Ȁ 1.3; nadir: 11.2 Ȁ 1.0; peak: 24.6 Ȁ 1.6 ng/mL) (P 0.01), whereas the remaining 10 patients with a glucose nadir of 76 Ȁ 2 mg/dL had no increase in adrenal steroids. Both glucose and protein suppressed ghrelin (from 935 Ȁ 57 to 777 Ȁ 51 pg/mL and from 948 Ȁ 60 to 816 Ȁ 61 pg/mL, respectively). After glucose ingestion, ghrelin returned to baseline by 4 h and increased to 1094 Ȁ 135 pg/mL at 5 h. After the protein challenge, ghrelin remained below the baseline (872 Ȁ 60 pg/mL) even at 5 h. The overall treatment effect was highly significant (P 0.0001). Conclusions: Glucose ingestion caused significantly more hyperinsulinemia than did protein, and it stimulated cortisol and DHEA. Protein intake suppressed ghrelin significantly longer than did glucose, which suggested a prolonged satietogenic effect. These findings provide mechanistic support for increasing protein intake and restricting the simple sugar intake in a PCOS diet.Am J Clin Nutr 2007;85:688 -94.

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Section: Discussionmentioning

confidence: 83%

Relation of nutrients and hormones in polycystic ovary syndrome

Kasim-Karakas

Cunningham

Tsodikov

2007

The American Journal of Clinical Nutrition

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“…DHEA increases glucose uptake in hepatocytes (as shown by the increased uptake of 2-deoxyglucose) and increases insulin binding to its own receptor (11,12). Conversely, elevated circulating levels of glucose or insulin may cause a decrease in DHEAS levels, potentially by glucose or insulin action on the adrenal gland itself (35). Glucose-mediated glucose disposal, or the ability of glucose to control its own production and uptake, has been suggested as a possible mechanism of excess androgens in PCOS (34).…”

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone sulfate and insulin resistance in patients with polycystic ovary syndrome

Brennan

Huang

Azziz

2009

Fertility and Sterility

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“…DHEAS levels were not measured [76]. We studied nine reproductive-aged patients with PCOS and nine age, race, and BMI-matched controls with an insulin-modified FSIVGTT and an acute 60 min ACTH-(1-24) stimulation test [77]. The insulin sensitivity index (S I ) and the acute insulin response to glucose (AIR G ) had a limited correlation with adrenocortical parameters in both groups.…”

Section: B) Effect Of Abnormalities Of the Glucose/insulin Axismentioning

confidence: 99%

The adrenal and polycystic ovary syndrome

Yildiz

Azziz

2007

Rev Endocr Metab Disord

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112

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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.

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Glucose action and adrenocortical biosynthesis in women with polycystic ovary syndrome

Cited by 40 publications

References 40 publications

Relation of nutrients and hormones in polycystic ovary syndrome

Relation of nutrients and hormones in polycystic ovary syndrome

Dehydroepiandrosterone sulfate and insulin resistance in patients with polycystic ovary syndrome

The adrenal and polycystic ovary syndrome

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