Impact of glycemic variations on the regulation of androgen metabolism in obese women with polycystic ovary syndrome  

Oleh:

Ludwig, Annika K. ; Goharian, Lilian G. ; Dietze, Theresa ; Tauchert, Sacha

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 92 no. 01 (Jul. 2009), page 271-276.
Topik: PCOS; obesity; androgen; hypoglycemia; hyperglycemia; glucose; clamp study; insulin

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2009.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective : To assess the influence of alterations in glucose concentrations on androgen levels in patients with polycystic ovary syndrome (PCOS) and in healthy controls. Design : Prospective, controlled study. Setting : Tertiary care center. Patient(s) : Seven patients with PCOS and 20 healthy controls. Intervention(s) : Hyperinsulinemic glucose clamp study with stepwise reduction of the plasma glucose level from hyperglycemia to hypoglycemia. Main Outcome Measure(s) : Concentrations of insulin, C-peptide, cortisol, T, androstenedione, 17-hydroxyprogesterone, DHEA, and DHEAS during hyperglycemia, euglycemia, and hypoglycemia. Result(s) : Total T levels and the free androgen index were significantly higher in the PCOS group at baseline and throughout the clamp. The levels of T, androstenedione, DHEAS, and 17-hydroxyprogesterone were not influenced by short-term changes of plasma glucose concentrations in both groups. However, hypoglycemia led to a significant increase in DHEA levels in PCOS patients as well as in controls. Cortisol levels were not increased during hypoglycemia in either group. Conclusion(s) : In contrast to men, androgen levels are not influenced by short-term changes of plasma glucose levels in PCOS patients and in healthy women. However, DHEA concentrations increase with decreasing glucose levels independently from an activation of the hypothalamic–pituitary–adrenal axis. This supports a gender difference regarding the counterregulatory hormone response to hypoglycemia.

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