Human apolipoprotein A-II associates with triglyceride-rich lipoproteins in plasma and impairs their catabolism |
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Authors: | Dugué-Pujol Sonia Rousset Xavier Pastier Danièle Quang Nhuan Tran Pautre Virginie Chambaz Jean Chabert Michèle Kalopissis Athina-Despina |
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Institution: | Institut National de la Santé et de la Recherche Médicale, Unité Mixte de Recherche 505, Paris, F-75006 France. |
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Abstract: | Postprandial hypertriglyceridemia and low plasma HDL levels, which are principal features of the metabolic syndrome, are displayed by transgenic mice expressing human apolipoprotein A-II (hapoA-II). In these mice, hypertriglyceridemia results from the inhibition of lipoprotein lipase and hepatic lipase activities by hapoA-II carried on VLDL. This study aimed to determine whether the association of hapoA-II with triglyceride-rich lipoproteins (TRLs) is sufficient to impair their catabolism. To measure plasma TRL residence time, intestinal TRL production was induced by a radioactive oral lipid bolus. Radioactive and total triglyceride (TG) were rapidly cleared in control mice but accumulated in plasma of transgenic mice, in relation to hapoA-II concentration. Similar plasma TG accumulations were measured in transgenic mice with or without endogenous apoA-II expression. HapoA-II (synthesized in liver) was detected in chylomicrons (produced by intestine). The association of hapoA-II with TRL in plasma was further confirmed by the absence of hapoA-II in chylomicrons and VLDL of transgenic mice injected with Triton WR 1339, which prevents apolipoprotein exchanges. We show that the association of hapoA-II with TRL occurs in the circulation and induces postprandial hypertriglyceridemia. |
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Keywords: | postprandial hypertriglyceridemia transgenic mice apolipoprotein A-II knockout mice chylomicrons very low density lipoprotein plasma residence time |
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