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Increased number of IGF‐I receptors on erythrocytes of women with polycystic ovarian syndrome
Author(s) -
Gdansky E.,
Diamant Y. Z.,
Laron Z.,
Silbergeld A.,
Kaplan B.,
Eshet R.
Publication year - 1997
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1997.2251043.x
Subject(s) - endocrinology , medicine , hyperandrogenism , receptor , androstenedione , insulin , basal (medicine) , polycystic ovary , hyperinsulinemia , hyperinsulinism , biology , insulin resistance , androgen , hormone
OBJECTIVE To test the hypothesis that insulin acts though ovarian IGF‐I receptors to produce excessive amounts of androgens in polycystic ovarian syndrome (PCOS), by measuring the binding capacity of IGF‐I receptors on erythrocytes and relating the findings to the degree of hyperandrogenism and hyperinsulinaemia. DESIGN A case‐control study of IGF‐I receptors on erythrocytes of women with PCOS and age‐ and weight‐matched controls. PATIENTS AND METHODS IGF‐I receptors on erythrocytes, serum levels of androgens, IGF‐I, GH, basal insulin and insulin response during oral glucose tolerance test (oGTT) were measured after induced or spontaneous withdrawal bleeding in 10 women with PCOS and eight normo‐ovulatory women. RESULTS An increased number of IGF‐I receptors was found on erythrocytes of patients with PCOS compared with the controls ( P < 0.01), irrespective of their body mass index. Serum IGF‐I levels were similar in both groups. The degree of hyperinsulinaemia, provoked by oGTT, correlated positively with basal insulin ( r = 0.69; P = 0.003), but not with the number of IGF‐I receptors. However, the number of IGF‐I receptors correlated positively with androstenedione ( r = 0.54, P = 0.0018). CONCLUSIONS The findings in the present study that the number of IGF‐I receptors and not the insulin levels correlate with serum androstenedione support the theory that the hyperandrogenism in PCOS is not a direct effect of the hyperinsulinaemia, but IGF‐I mediated.