16 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
Early Detection and Treatment of Altered Growth and Puberty in Children and Adolescents with Vertically-Acquired Hiv-1 Infection: It's Time to Think about it
Consensus statement - Prader-Willi syndrome: Growth hormone (GH)/insulin-like growth factor axis deficiency and GH treatment
Prader-Willi syndrome (PWS) is a disabling condition characterized by hypotonia, hyperphagia, obesity, short stature, delayed or absent puberty, and mental retardation. The syndrome complex was first described in 1956 by Dr. Andrea Prader and colleagues [1]. In the 1980s, a characteristic genetic defect was identified involving deletion of paternal alleles at chromosome 15q11-13 [2-6]. This occurs by deletion of alleles on the paternal copy of chromosome 15q, an absent paternal chromosome 15q with maternal disomy, or, rarely, by mutations of the imprinting center of chromosome 15q. The estimated population prevalence of PWS is 1 in 15,000 live births
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The insulin-like growth factor binding protein BP-25 is expressed by human breast cancer cells
Specific binding proteins are thought to modulate the effects of IGF-I. Previous work has demonstrated that media conditioned by human breast cancer cells contains IGF-I binding activity. Radiolabelled IGF-I incubated with serum-free conditioned media from the breast cancer cell line MDA-MB 231 eluted with an apparent M.W. of 35–40 kDa when analyzed by gel filtration chromatography at pH 7.4. The M.W. of this binding activity corresponded to that of BP-25, a binding protein cloned from the hepatocellular carcinoma cell line HepG2. Two breast cancer cell lines, MDA-MB 231 and Hs578T, were found to express BP-25 RNA. Specific BP-25 radioimmunoassay detected BP-25 production in the conditioned media of these two cell lines. Immunoprecipitation confirmed that metabolically labelled MDA-MB 231 released 30 kDa BP-25 into its medium. This study demonstrates that some breast cancer cells express the IGF-I binding protein, BP-25