Microsomal triglyceride transfer protein (MTP)
What it does, reaction by reaction
Lipoprotein Metabolism (Exogenous and Endogenous Pathways: chylomicrons, VLDL, LDL, HDL) Lipid Metabolism · Intestine, liver, plasma, capillary endothelium
Nascent chylomicron assembly: TAG/cholesteryl ester + apoB-48 → chylomicron
Converts TAG/cholesteryl ester ApoB-48 into Chylomicron
› Notes
Microsomal triglyceride transfer protein (MTP) loads lipids onto newly translated apoB-48 in intestinal ER; further lipidation and Golgi processing create nascent chylomicrons. ApoB-48 is generated by intestinal APOB mRNA editing and is obligatory for particle assembly; MTP-mediated apoB lipidation is the critical assembly step. Chylomicrons enter lymph, then systemic plasma via the thoracic duct.
Hepatic TAG/cholesteryl ester + apoB-100 → nascent VLDL
Converts ApoB-100 into Nascent VLDL
› Notes
Hepatic MTP transfers lipids to full-length apoB-100 in ER; additional TAG lipidation produces VLDL, which is secreted into plasma. Availability of hepatic fatty acids from de novo lipogenesis, adipose NEFA influx, and dietary remnants controls VLDL-TAG output. ApoB-100 is required for VLDL assembly and later serves as the LDLR ligand.
Showing all 2 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Lipoprotein Metabolism (Exogenous and Endogenous Pathways: chylomicrons, VLDL, LDL, HDL)
ApoB synthesis and luminal lipid availability
MTP inhibitors; severe lipid shortage
Insulin resistance and hepatic fatty-acid influx can increase VLDL production; regulation is largely transcriptional/substrate-driven
Recent literature
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