3 research outputs found
Elevated serum levels of free insulin-like growth factor I in polycystic ovary syndrome
Polycystic ovary syndrome (PCOS) is the most common cause of anovulation
in women. Previous studies suggest that the pathogenesis of PCOS may
involve interrelated abnormalities of the insulin-like growth factor (IGF)
and ovarian steroidogenesis systems. We investigated this hypothesis in
fasting serum samples from 140 women with PCOS (age, 27.4 +/- 0.4 yr; body
mass index, 26.3 +/- 0.5 kg/m2; mean +/- SEM). IGF-related parameters were
also studied in a group of normoovulatory women (n = 26; age, 26 +/- 4 yr;
body mass index, 23.6 +/- 4.3 kg/m2). For the PCOS group, the mean
testosterone (T) level was 2.5 +/- 0.1 nmol/L, and it was significantly
correlated with LH (r = 0.41; P < 10(-6)), estrone (r = 0.33; P = 0.016),
estradiol (r = 0.18; P = 0.04), and androstenedione (AD; P < 10(-6)), but
not with dehydroepiandrosterone sulfate (P = 0.71), a marker of adrenal
steroidogenesis. T and AD were also related to total ovarian follicle
number and ovarian size, as previously found with normoovulatory women
(1). There were no differences between the PCOS subjects and the
normoovulatory group for total IGF-I, IGF-II, or IGF-binding protein-3
(IGFBP-3). However, IGFBP-1 levels were significantly decreased in the
PCOS group (1.0 +/- 0.2 vs. 7.3 +/- 1.1 ng/mL; P < 0.001) and were
inversely correlated with serum insulin levels (r = -0.50; P < 10(-8)).
Serum levels of free IGF-I (fIGF-I) were elevated (5.9 +/- 0.3 vs. 2.7 +/-
0.3 ng/mL; P < 0.001) in inverse relation with IGFBP-1 (r = -0.31; P =
0.046). Serum fIGF-I levels were related to total follicle number (r = -
0.35; P < 10(-4)) and to the ratio of sex hormone-binding globulin to T (r
= -0.23; P = 0.009). However, these relationships were not independent of
other variables. Despite the more than 2-fold elevation in fIGF-I levels,
significant relationships between fIGF-I and markers of ovarian
steroidogenesis (T, AD, estradiol, and estrone) could not be demonstrated.
In conclusion, although we confirmed correlations between LH and
hyperandrogenemia and have found abnormalities in the IGF system in a
large cohort of PCOS subjects, a direct relationship between
hyperandrogenism and the IGF system could not be shown. Previous studies
suggest that elevated LH and hyperinsulinemia lead to excess ovarian
androgen synthesis in PCOS and that the intraovarian IGF system is
important for normal follicle development and may be important in the
arrested state of follicle development in PCOS. However, the data
presented in this cross-sectional study suggest that insulin-related
changes in circulating IGFBP-1 and subsequent elevation of fIGF-I reflect
insulin resistance and have little enhancing effects on ovarian
steroidogenesis in this disorder