PMID- 10844597 OWN - NLM STAT- MEDLINE DCOM- 20000824 LR - 20061115 IS - 0085-2538 (Print) IS - 0085-2538 (Linking) VI - 57 IP - 6 DP - 2000 Jun TI - Estrogen effects on triglyceride metabolism in analbuminemic rats. PG - 2268-74 AB - BACKGROUND: Triglyceride (TG) levels are normally lower in female rats, while the opposite is the case in the Nagase analbuminemic rats (NAR). Increased 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 testosterone causes hypertriglyceridemia in this strain. The mechanism for this increase is unknown. METHODS: We measured secretion of very-low density lipoprotein (VLDL) TG using Triton WR 1339 clearance as the disappearance from blood of 3H-trioleate and 14C-cholesterol-labeled chylomicrons (CM), and the activity of the PH lipases: LpL and hepatic lipase (HL). All were determined in Sprague-Dawley (SD) and NAR female, male, and ovariectomized (OVX) rats. RESULTS: TG levels were significantly greater in female NAR in comparison to all other groups. Ovariectomy of NAR significantly ameliorated hypertriglyceridemia. VLDL TG secretion was significantly greater in intact female NAR compared with all other groups. There were no other differences in VLDL TG secretion among the other groups. The clearance of CM was greatest in female SD rats, and OVX had no effect. NAR cleared CM less well than did SD rats (P < 0.001), but among NAR, clearance was greatest in OVX NAR and male NAR (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-mediated 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. FAU - Shearer, G C AU - Shearer GC AD - Division of Nephrology, Department of Medicine UC Davis, Davis, California 95616, USA. FAU - Joles, J A AU - Joles JA FAU - Jones, H AU - Jones H FAU - Walzem, R L AU - Walzem RL FAU - Kaysen, G A AU - Kaysen GA LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. PL - United States TA - Kidney Int JT - Kidney international JID - 0323470 RN - 0 (Chylomicrons) RN - 0 (Estrogens) RN - 0 (Lipoproteins, VLDL) RN - 0 (Serum Albumin) RN - 0 (Triglycerides) RN - 9005-49-6 (Heparin) RN - EC 3.1.1.3 (Lipase) RN - EC 3.1.1.34 (Lipoprotein Lipase) SB - IM MH - Animals MH - Blood/metabolism MH - Chylomicrons/blood MH - Estrogens/*physiology MH - Female MH - Heparin/pharmacology MH - Lipase/blood MH - Lipoprotein Lipase/metabolism MH - Lipoproteins, VLDL/blood MH - Liver/enzymology MH - Male MH - Ovariectomy MH - Rats MH - Rats, Mutant Strains MH - Rats, Sprague-Dawley MH - Serum Albumin/*analysis MH - Triglycerides/*blood EDAT- 2000/06/09 09:00 MHDA- 2000/08/29 11:01 CRDT- 2000/06/09 09:00 PHST- 2000/06/09 09:00 [pubmed] PHST- 2000/08/29 11:01 [medline] PHST- 2000/06/09 09:00 [entrez] AID - S0085-2538(15)46987-X [pii] AID - 10.1046/j.1523-1755.2000.00087.x [doi] PST - ppublish SO - Kidney Int. 2000 Jun;57(6):2268-74. doi: 10.1046/j.1523-1755.2000.00087.x.