TY - JOUR
T1 - Polycystic ovaries in non-obese and obese patients
T2 - Possible pathophysiological mechanism based on new interpretation of facts and findings
AU - Insler, V.
AU - Shoham, Z.
AU - Barash, A.
AU - Koistinen, R.
AU - Seppälä, M.
AU - Hen, M.
AU - Lunenfeld, B.
AU - Zadik, Z.
PY - 1993/3
Y1 - 1993/3
N2 - This study was designed to investigate the basic concentrations of different hormones in obese and non-obese patients with polycystic ovarian disease (PCOD). Eight women with PCOD, of whom four were obese with body mass index (BMI, kg/m2) of >25 and four were non-obese with BMI <25, volunteered to participate in this study. Serum samples were taken every 20 min over an 8 h period, starting at 2300 h, on day 5 of a spontaneous or gestagen-induced cycle. Basic insulin concentration was found to be significantly higher in the obese women compared with their non-obese counterparts (P < 0.0001). Serum concentrations of insulin-like growth factor binding protein (IGFBP-I) and sex hormone binding globulin (SHBG) were found to be significantly lower (P < 0.001 for both hormones) in the obese compared with the non-obese women. Serum concentrations of insulin-like growth factor I (IGF-I) did not differ between the two groups. The non-obese women had significantly higher serum concentrations of luteinizing hormone (LH) (P < 0.001) and of growth hormone (GH) (P < 0.002) than their obese counterparts. Based on these results, two models of the development of PCOD were suggested. In obese women, hyperinsulinaemia causes an excessive production of androgens through the enhancement of IGF-I receptors which, in synergism with LH, causes increased activity of cytochrome P-450c 17a. In non-obese patients, relative increase of GH concentration stimulates excessive ovarian IGF-I production. At this point synergism with LH results in excessive production of androgens by the same mechanism as in obese patients. The increase in androgen may lead to changes in important brain centres, which might cause a disturbance in gonadogrophin secretion leading to the typical changes of PCOD.
AB - This study was designed to investigate the basic concentrations of different hormones in obese and non-obese patients with polycystic ovarian disease (PCOD). Eight women with PCOD, of whom four were obese with body mass index (BMI, kg/m2) of >25 and four were non-obese with BMI <25, volunteered to participate in this study. Serum samples were taken every 20 min over an 8 h period, starting at 2300 h, on day 5 of a spontaneous or gestagen-induced cycle. Basic insulin concentration was found to be significantly higher in the obese women compared with their non-obese counterparts (P < 0.0001). Serum concentrations of insulin-like growth factor binding protein (IGFBP-I) and sex hormone binding globulin (SHBG) were found to be significantly lower (P < 0.001 for both hormones) in the obese compared with the non-obese women. Serum concentrations of insulin-like growth factor I (IGF-I) did not differ between the two groups. The non-obese women had significantly higher serum concentrations of luteinizing hormone (LH) (P < 0.001) and of growth hormone (GH) (P < 0.002) than their obese counterparts. Based on these results, two models of the development of PCOD were suggested. In obese women, hyperinsulinaemia causes an excessive production of androgens through the enhancement of IGF-I receptors which, in synergism with LH, causes increased activity of cytochrome P-450c 17a. In non-obese patients, relative increase of GH concentration stimulates excessive ovarian IGF-I production. At this point synergism with LH results in excessive production of androgens by the same mechanism as in obese patients. The increase in androgen may lead to changes in important brain centres, which might cause a disturbance in gonadogrophin secretion leading to the typical changes of PCOD.
KW - Growth hormone
KW - Insulin
KW - Insulin-like growth factor binding-protein I
KW - Obesity polycystic ovaries
UR - http://www.scopus.com/inward/record.url?scp=0027394943&partnerID=8YFLogxK
U2 - 10.1093/oxfordjournals.humrep.a138055
DO - 10.1093/oxfordjournals.humrep.a138055
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C2 - 7682564
AN - SCOPUS:0027394943
SN - 0268-1161
VL - 8
SP - 379
EP - 384
JO - Human Reproduction
JF - Human Reproduction
IS - 3
ER -