The aetiology of the polycystic ovarian syndrome together with new adv
ances in the molecular genetics and possible candidate genes for the i
nheritance of the syndrome is discussed. The possible role of leptin i
n the obesity of polycystic ovarian syndrome is reviewed. Hyperinsulin
aemia acts not only as the trigger for hyperandrogenaemia and infertil
ity, but also by stimulating plasminogen activator inhibitor type 1; h
yperinsulinaemia may also promote atherogenesis in polycystic ovarian
syndrome. The long-term effects of the metabolic derangements accompan
ying hyperinsulinaemia are reviewed. Special emphasis is placed on the
use of novel insulin sensitizers such as troglitazone which promise n
ew treatment opportunities in polycystic ovarian syndrome for both fer
tility and long-term disease prevention. (C) 1998 Lippincott-Raven Pub
lishers.