| Autor: |
Jeltje R. Goudriaan, Marion A.M. den Boer, Patrick C.N. Rensen, Maria Febbraio, Folkert Kuipers, Johannes A. Romijn, Louis M. Havekes, Peter J. Voshol |
| Jazyk: |
angličtina |
| Rok vydání: |
2005 |
| Předmět: |
|
| Zdroj: |
Journal of Lipid Research, Vol 46, Iss 10, Pp 2175-2181 (2005) |
| Druh dokumentu: |
article |
| ISSN: |
0022-2275 |
| DOI: |
10.1194/jlr.M500112-JLR200 |
| Popis: |
CD36 is involved in high-affinity peripheral FFA uptake. CD36-deficient (cd36−/−) mice exhibit increased plasma FFA and triglyceride (TG) levels. The aim of the present study was to elucidate the cause of the increased plasma TG levels in cd36−/− mice. cd36−/− mice showed no differences in hepatic VLDL-TG production or intestinal [3H]TG uptake compared with wild-type littermates. cd36−/− mice showed a 2-fold enhanced postprandial TG response upon an intragastric fat load (P < 0.05), with a concomitant 2.5-fold increased FFA response (P < 0.05), suggesting that the increased FFA in cd36−/− mice may impair LPL-mediated TG hydrolysis. Postheparin LPL levels were not affected. However, the in vitro LPL-mediated TG hydrolysis rate as induced by postheparin plasma of cd36−/− mice in the absence of excess FFA-free BSA was reduced 2-fold compared with wild-type plasma (P < 0.05). This inhibition was relieved upon the addition of excess FFA-free BSA. Likewise, increasing plasma FFA in wild-type mice to the levels observed in cd36−/− mice by infusion prolonged the plasma half-life of glycerol tri[3H]oleate-labeled VLDL-like emulsion particles by 2.5-fold (P < 0.05).We conclude that the increased plasma TG levels observed in cd36−/− mice are caused by decreased LPL-mediated hydrolysis of TG-rich lipoproteins resulting from FFA-induced product inhibition of LPL. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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