Background. Triglyceride (TG) levels are normally lower in female rats, whi
le the opposite is the case in the Nagase analbuminemic rats (NAR). Increas
ed TG levels in normal males are caused by a testosterone-mediated decrease
in postheparin (PH) lipoprotein lipase (LpL). Castration of males reduces
TG, while castration of females is without effect. TG levels are reduced by
castration of the female NAR, suggesting that estrogen rather than testost
erone causes hypertriglyceridemia in this strain. The mechanism for this in
crease is unknown.
Methods. We measured secretion of very-low density lipoprotein (VLDL) TG us
ing Triton WR 1339 clearance as the disappearance from blood of H-3-triolea
te and C-14-cholesterol-labeled chylomicrons (CM), and the activity of the
PH lipases: LpL and hepatic lipase (HL). All were determined in Sprague-Daw
ley (SD) and NAR female, male, and ovariectomized (OVX) rats.
Results. TG levels were significantly greater in female NAR in comparison t
o all other groups. Ovariectomy of NAR significantly ameliorated hypertrigl
yceridemia. VLDL TG secretion was significantly greater in intact female NA
R compared with all other groups. There were no other differences in VLDL T
G secretion among the other groups. The clearance of CM was greatest in fem
ale SD rats, and OVX had no effect. NAR cleared CM less well than did SD ra
ts (P < 0.001), but among NAR, clearance was greatest in OVX NAR and male N
AR (P < 0.002). Both PH LpL activity and HL activity were lowest in female
NAR (P < 0.05). Ovariectomy partially corrected the defect in HL (P < 0.05)
.
Conclusion. TG levels in female NAR are in part a result of increased VLDL-
TG secretion, an effect mediated by estrogen. The presence of an estrogen-m
ediated catabolic defect that was alleviated by OVX was also observed. This
catabolic defect is likely a result of an estrogen-mediated decrease both
in LpL and HL expressed only in the presence of analbuminemia.