Key result
Inhibition of adrenal hepatic lipase in rats increased adrenal SR-BI mRNA 5.2-fold and mass 1.6-fold, and increased adrenal uptake of rat HDL-cholesteryl ether by 68% at 4 hours.
Why the study?
Does acute in vivo inhibition of hepatic lipase increase SR-BI expression and HDL-cholesteryl ether uptake in rat adrenal glands?
Does acute in vivo inhibition of hepatic lipase increase SR-BI expression and HDL-cholesteryl ether uptake in rat adrenal glands?
Hepatic lipase activity is not required for SR-BI-mediated HDL-cholesteryl ester uptake by rat adrenal glands, and its inhibition upregulates SR-BI expression.
Answers are grounded in this paper and cite their sources.
Rat adrenal findings should not change practice; hypothesis-generating for SR-BI regulation in human HDL metabolism.
Hepatic lipase (HL) and scavenger receptor type B class I (SR-BI) have both been implicated in high density lipoprotein (HDL)-cholesteryl ester uptake in cholesterol-utilizing tissues. Inactivation of HL by gene-directed targeting in mice results in up-regulation of SR-BI expression in adrenal gland (Wang, N., Weng, W., Breslow, J. L., and Tall, A. R. (1996) J. Biol. Chem. 271, 21001-21004). The net effect on HDL-cholesteryl ester uptake is not known. We determined the impact of acute in vivo inhibition of rat adrenal HL activity by antibodies on SR-BI expression and on human and rat HDL-[3H]cholesteryl ether (CEth) uptake in the adrenal gland. Rat HDL was isolated from rats in which HL activity had been inhibited for 1 h. The rats were studied under basal conditions (not ACTH-treated) and after previous treatment with ACTH for 6 days (ACTH-treated). Intravenous injection of anti-HL resulted in 70% lowering of adrenal HL activity in both conditions which were maintained for at least 8 h. In not ACTH-treated rats, inhibition of adrenal HL increased adrenal SR-BI mRNA (5.2-fold) and mass (1. 6-fold) within 4 h. HL inhibition resulted in 41% and 14% more adrenal accumulation of human HDL-[3H]CEth during 4 and 24 h, respectively. The adrenal uptake of rat HDL-[3H]CEth increased by 68%, 4 h after the antibody injection. ACTH treatment increased total adrenal HL activity from 3.7 +/- 0.5 milliunits to 34.0 +/- 17. 2 milliunits, as well as adrenal SR-BI mRNA from 2.9 +/- 0.7 arbitrary units (A.U.) to 86.8 +/- 41.1 A.U. and SR-BI mass from 7.7 +/- 1.8 A.U. to 63.16 +/- 46.7 A.U. The human HDL-[3H]CEth uptake by adrenals was also significantly increased from 0.58 +/- 0.11% of injected dose to 7.24 +/- 1.58% of injected dose. Inhibition of adrenal HL activity did not result in further induction of SR-BI expression and did not affect human HDL-[3H]CEth uptake. These findings indicate that SR-BI expression may be influenced by changes in HL activity. HL activity is not needed for the SR-BI-mediated HDL-cholesteryl ester uptake by rat adrenal glands.
No takes yet. Share an insight, caveat, or question.
Bruggen et al. (1998) studied this question. In vivo inhibition of hepatic lipase (HL) by antibodies vs. Uninhibited state was evaluated on Adrenal SR-BI expression and HDL-cholesteryl ether uptake. Inhibition of adrenal hepatic lipase in rats increased adrenal SR-BI mRNA 5.2-fold and mass 1.6-fold, and increased adrenal uptake of rat HDL-cholesteryl ether by 68% at 4 hours.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: