V. Markussis et al., THE ROLE OF INSULIN IN OVARIAN SIZE IN PATIENTS WITH THE POLYCYSTIC-OVARY-SYNDROME, Gynecological endocrinology, 8(3), 1994, pp. 197-202
The objective of this study was to evaluate whether the degree of supp
ression of ovarian volume effected by a gonadotropin releasing hormone
(GnRH) agonist in patients with polycystic ovary syndrome (PCOS) corr
elated with basal insulin secretion and insulin secretion provoked by
a glucose challenge. Eighteen PCOS patients received the GnRH agonist
D-tryptophan-6-LHRH (Decapeptyl, 3.75 mg monthly i.m.) for 6 months an
d had blood glucose and insulin measured during a 75 g oral glucose to
lerance test (OGTT) prior to and at the end of therapy. According to o
varian volume suppression after GnRH agonist therapy, two groups were
defined: in group A (n = 10; mean body mass index (BMI) +/- SEM, 25.6
+/- 1.6 kg/m2) ovarian volume regressed from 17.9 +/- 1.6 to 6.7 +/- 0
.3 ml (full responders) and in group B (n = 8; mean BMI +/- SEM, 28.1
+/- 2.3 kg/m2) from 21.5 +/- 1.1 to 15.1 +/- 1.0 ml (partial responder
s). Results showed that GnRH agonist therapy did not affect significan
tly BMI or fasting levels and area under the curve (AUC) for glucose a
nd insulin in the respective groups. Fasting insulin levels correlated
positively with ovarian volume prior to (r = 0.56, p < 0.05) and afte
r 6 months of GnRH agonist therapy (r = 0.80, p < 0.005). The suppress
ibility of ovarian volume with GnRH agonist therapy correlated negativ
ely with the difference between maximal and basal levels (r = -0.68),
the area under the curve (r = -0.62) and maximal levels (r = -0.72) fo
r insulin during the OGTT. This study shows that insulin output per se
seems to be an important determinant of ovarian volume in women with
PCOS. Furthermore, it would appear that GnRH analogues are less effect
ive in reducing ovarian volume in patients with excessive insulin secr
etion.