Serum Resistin and Plasma Visfatin: Relation to Insulin Resistance and Hyperandrogenism in Women with Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a heterogeneous syndrome characterized by
hyperandrogenismand insulin resistance. The mechanism that is responsiblefor
insulin resistance is unclearand several hypotheses havebeen suggested. Resistin,
and visfatin, a new protein with potential insulin-mimetic action are adipokines which
are suggested to play a role in the pathogenesis of insulin resistance. The aim of the
study is to assess the relationship between both serum resistin and plasma visfatin
and insulin resistance and hyperandrogenism in PCOS patients. The present study
included 60 women with polycystic ovary syndrome (PCOS) (group II: 30 with BMI <
25 kg/m
2
and group IV: 30 with BMI > 25 kg/m
2
) and 20 healthy women (group I: 10
with BMI < 25 kg/m
2
and group III: 10 with BMI > 25 kg/m
2
) served as controls.
Fasting blood samples were withdrawn between the 3
rd
and the 6
th
day of the
menstrual cycle of the ovulating women and between the 3
rd
and the 6
th
day of a
spontaneous bleeding of the anovulatory women. Serum LH, FSH free testosterone,
resistin, plasma glucose, insulin and visfatin were estimated in all patients and
controls. Insulin resistance was assessed using the homeostatic assessment model
(HOMA). Resistin and visfatin levels were significantly higher in women with PCOS
(13.26±7.58 ng/ml and 35.82±8.94 ng/ml) than normal controls (7.95± 2.17 ng/ml
and 11.88±1.84 ng/ml) (p=0.003, p<0.0001), respectively. Serum resistin levels in
groups III and IV were significantly higher compared to groups I and II (p< 0.001,
p< 0.001) being higher in group IV, whereas no significant difference existed between
groups I and II. Resistin correlated positively with BMI, fasting plasma glucose,
fasting plasma insulin and HOMA index in women with BMI > 25 kg/ m
2
(groups III
and IV).In other words, resistin was found tocorrelate significantlywith all obesity-associated parameters. Plasma visfatin levels were significantly higher in groups II
and IV being higher in group IV when compared to the control groups I and III,
whereas no significant difference existed between control groups I and III. Visfatin
also positively correlated with, fasting plasma insulin (r = 0.882, p< 0.01 and r =
0.952, p< 0.01) and HOMA (r = 0.908, p< 0.01 and r = 0.942, p< 0.01) in women
with PCOS (groups II and IV), respectively. In women with PCOS (groups II and IV),
both resistin and visfatin positively correlated with free testosterone (r =0.6, p =
0.003 and r = 0.973, p< 0.01) and (r = 0.969, p<0.01 and r = 0.922, p<0.01),
respectively. In women with PCOS (groupsII and IV), resistin correlated positively
with visfatin (r = 0.784, p< 0.01, r =0.954, p< 0.01), respectively. From the current
data, it could be suggested that resistin levels correlate with insulin resistance as a
consequence of obesity itself, rather than a, causative factor. Also the possibility that
resistin may play a role in augmenting androgen biosynthesis in women with PCOS
could arise. We presume that, in PCOS the increase in plasma visfatin is a secondary
event in order to prevent further development of insulin resistance. Finally, the
insulin-like visfatin action might stimulate ovarian androgen synthesis and secretion
and thus contribute to the pathogenesis of PCOS.