| First Author | Dichek HL | Year | 2004 |
| Journal | J Lipid Res | Volume | 45 |
| Issue | 3 | Pages | 551-60 |
| PubMed ID | 14679168 | Mgi Jnum | J:88634 |
| Mgi Id | MGI:3036409 | Doi | 10.1194/jlr.M300459-JLR200 |
| Citation | Dichek HL, et al. (2004) The bridging function of hepatic lipase clears plasma cholesterol in LDL receptor-deficient 'apoB-48-only' and 'apoB-100-only' mice. J Lipid Res 45(3):551-60 |
| abstractText | Hepatic lipase clears plasma cholesterol by lipolytic and nonlipolytic processing of lipoproteins. We hypothesized that the nonlipolytic processing (known as the bridging function) clears cholesterol by removing apoB-48- and apoB-100-containing lipoproteins by whole particle uptake. To test our hypotheses, we expressed catalytically inactive human HL (ciHL) in LDL receptor deficient 'apoB-48-only' and 'apoB-100-only' mice. Expression of ciHL in 'apoB-48-only' mice reduced cholesterol by reducing LDL-C (by 54%, 46 +/- 6 vs. 19 +/- 8 mg/dl, P < 0.001). ApoB-48 was similarly reduced (by 60%). The similar reductions in LDL-C and apoB-48 indicate cholesterol removal by whole particle uptake. Expression of ciHL in 'apoB-100-only' mice reduced cholesterol by reducing IDL-C (by 37%, 61 +/- 19 vs. 38 +/- 12 mg/dl, P < 0.003). Apo-B100 was also reduced (by 27%). The contribution of nutritional influences was examined with a high-fat diet challenge in the 'apoB-100-only' background. On the high fat diet, ciHL reduced IDL-C (by 30%, 355 +/- 72 vs. 257 +/- 64 mg/dl, P < 0.04) but did not reduce apoB-100. The reduction in IDL-C in excess of apoB-100 suggests removal either by selective cholesteryl ester uptake, or by selective removal of larger, cholesteryl ester-enriched particles. Our results demonstrate that the bridging function removes apoB-48- and apoB-100-containing lipoproteins by whole particle uptake and other mechanisms. |
