From the Frank Rundle House. Royal Hospital for Women. 188 Oxford St, Paddington. 2021 New South Wales
Abstract: (6088 Views)
To assess the relative contribution of genetic and environmental factors
(particularly androgens) on circulating levels of lipid fractions, serum androgen
and lipid fractions were measured in 34 pairs of female-female twins aged from 15-
45 years, some of whom were discordant for polycystic ovary syndrome (PCOS)
diagnosed by ultrasound. Nineteen pairs were monozygotic twins (MZ) and 15
pairs were dizygotic twins (DZ). Five pairs of MZ and 6 pairs of DZ were
discordant for scan-PC a. We measured serum concentrations of total cholesterol
(TC), high density lipoprotein cholesterol (HDL-C), triglycerides (TRIG),
lipoprotein (a) [LP(a)], and apolipoprotein B (apo B). Also, testosterone (T),
dehydroepiandrosterone sulphate (DHEAS), sex hormone binding globulin (SHBG)
and 3a-androstanediol glucuronide (3a-diol G) levels were measured.
Transabdominal ultrasound was performed. Serum levels of TC, HDL-C, TRIG,
LP(a) and apo B in the twins with PCO were not significantly different from the
levels in their matched co-twins with normal ovaries. There were no significant
correlations between androgen-hormones including T, DHEAS and 3a-diol G
with any of the lipid measurements. Body mass index (BMI) was positively
correlated with TRIG, LP(a) (both p<0.05) and negatively correlated with HDLC
(p<0.001). SHBG was negatively correlated with TRIG and LP(a) and positively
associated with HDL-C (p<0.05). Insulin was significantly correlated with TRIG
(p<0.001) and negatively with HDL-C (p<0.01). The MZ intraclass correlation
exceeded that of the DZ for all the lipid variables measured. The heritability
estimates for LP(a), apo B, TC and HDL-C were 0.95, 0.56, 0.48 and 0.54,
respectively. However, the intraclass correlation coefficient for TRIG was not
significantly different between MZ and DZ but maximum likelihood analysis
indicated that at least 10% of the variance of circulating TRIG concentration is
determined by genetic factors. We conclude that twins discordant for pcas do not
have significantly different lipid profiles. We were unable to show any significant
effect of androgens on the lipid fractions measured. The results confirm that levels
of LP(a), HDL-C, TC and apo B are under significant genetic control and that this
is particularly so for LP(a). However, only 10% of the variation in TRIG levels
could be attributed to genetic influences after controlling for age and obesity.
Increase in BMI and insulin had a significant adverse effect on the lipid profile in
these female twins, effects which may enhance coronary risk.