AUTHOR=Lo Chunmin C. , Coschigano Karen T. TITLE=ApoB48 as an Efficient Regulator of Intestinal Lipid Transport JOURNAL=Frontiers in Physiology VOLUME=11 YEAR=2020 URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.00796 DOI=10.3389/fphys.2020.00796 ISSN=1664-042X ABSTRACT=

Fatty meals induce intestinal secretion of chylomicrons (CMs) containing apolipoprotein (Apo) B48. These CMs travel via the lymphatic system before entering the circulation. ApoB48 is produced after post-transcriptional RNA modification by Apobec-1 editing enzyme, exclusively in the small intestine of humans and most other mammals. In contrast, in the liver where Apobec-1 editing enzyme is not expressed (except in rats and mice), the unedited transcript encodes a larger protein, ApoB100, which is used in the formation of very low-density lipoproteins (VLDL) to transport liver-synthesized fat to peripheral tissues. Apobec-1 knockout (KO) mice lack the ability to perform ApoB RNA editing, and thus, express ApoB100 in the intestine. These mice, maintained on either a chow diet or high fat diet, have body weight gain and food intake comparable to their wildtype (WT) counterparts on the respective diet; however, they secrete larger triglyceride (TG)-rich lipoprotein particles and at a slower rate than the WT mice. Using a lymph fistula model, we demonstrated that Apobec-1 KO mice also produced fewer CMs and exhibited reduced lymphatic transport of TG in response to duodenal infusion of TG at a moderate dose; in contrast, the Apobec-1 KO and WT mice had similar lymphatic transport of TG when they received a high dose of TG. Thus, the smaller, energy-saving ApoB48 appears to play a superior role in comparison with ApoB100 in the control of intestinal lipid transport in response to dietary lipid intake, at least at low to moderate lipid levels.