Many organic compounds are taken up from the blood by membrane transporters, taken across the sinosuidal membrane of hepatocytes and then excreted into bile via the bile canalicular membrane. The hepatic uptake of conjugated bile acids is mediated by the sodium taurocholate cotransporting polypeptide. Many organic anions and bulky organic cations are incorporated into hepatocytes by the organic anion transporting polypeptide, while small organic cations are transported by the organic cation transporter. At the canalicular membrane, organic compounds are excreted into bile by ATP-binding cassette transporters which hydrolyse ATP to ADP. Excretion of monovalent bile acids is mediated by the canalicular bile salt transporter and that of organic anions, including divalent bile acid, conjugates, are mediated by the multi-drug resistance-associated protein 2, also termed canalicular multi-specific organic anion transporter. Organic cations are excreted into bile by the multi-drug resistance gene product (MDR) 1 and phospholipids are excreted by MDR3 (mdr2 in mice and rats). The clinical syndromes associated with alterations of these transporters are also discussed.

Molecular aspects of organic compound transport across the plasma membrane of hepatocytes.

Apolipoprotein E (apoE)-deficient mice develop hepatic steaatosis and show impaired very low density lipoprotein (VLDL)-triglyceride (TG) secretion. These effects are normalized on the introduction of the human APOE3 gene. To assess whether this apoE effect is isoform specific, we studied hepatic lipid metabolism in mice expressing either APOE3 or the mutant APOE3Leiden on apoe-/- or apoe+/- backgrounds. The transgenes were expressed mainly in periportal hepatocytes, as revealed by in situ hybridization. Mice expressing APOE3Leiden, on the apoe-/and apoe+/- backgrounds, had fatty livers, which were absent in APOE3/apoe-/- mice. APOE3Leiden/apoe-/mice showed a strongly reduced VLDL-TG secretion compared with APOE3/apoe-/- mice (48± 14 versus 82± 10 μmol/kg per hour, respectively). The presence of a single mouse apoe allele increased VLDL-TG secretion in APOE3Leiden/apoe +/- mice (121±43 μmol/kg per hour) compared with APOE3Leiden/apoe-/- mice. These results show that APOE3Leiden does not prevent development of a fatty liver and does not normalize VLDL-TG secretion in mice with an apoE-deficient background. The presence of a single mouse apoe allele is sufficient to normalize the APOE3Leiden-associated reduction of VLDL-TG secretion but does not prevent steatosis. We conclude that apoE-mediated stimulation of VLDL secretion is isoform specific. Chemicals/CAS: apolipoprotein E3 (Leidein); Apolipoprotein E3; Apolipoproteins B; Apolipoproteins E; Lipoproteins, VLDL; Protein Isoforms; RNA, Messenger; Triglycerides; very low density lipoprotein triglyceride

Mice Expressing Only the Mutant APOE3Leiden Gene Show Impaired VLDL Secretion

https://publications.tno.nl/publication/34625852/VxXGTb/mensenkamp-1999-apolipoprotein.pdf

Apolipoprotein E Participates in the Regulation of Very Low Density Lipoprotein-Triglyceride Secretion by the Liver

Impaired production of very low density lipoproteins (VLDL) by apolipoprotein E-deficient mouse hepatocytes in primary culture

Strong induction of MDR2 P-glycoprotein expression in livers of simvastatin-treated rats.

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Impaired production of very low density lipoproteins (VLDL) by apolipoprotein E-deficient mouse hepatocytes in primary culture

Strong induction of MDR2 P-glycoprotein expression in livers of simvastatin-treated rats.