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UID:20260806T073837EDT-4235rOvJcD@132.216.98.100
DTSTAMP:20260806T113837Z
DESCRIPTION:Dr. Zemin Yao\nDepartment of Biochemistry\, Microbiology and Im
 munology\, Ottawa\nInstitute of Systems Biology\, University of Ottawa\, C
 anada\n\n“New insight into an intrahepatic role of human apoC-III in\nhype
 rlipidemia and hepatic stress induced by lipotoxicity”\nThe plasma concent
 ration of human apoC-III is positively\nassociated with VLDL apoB-100 and 
 triglyceride (TG)\; elevated\napoC-III is invariably linked to hypertrigly
 ceridemia in humans and\ntransgenic mice. Although the hyperlipidemic role
  of apoC-III was\nascribed for its action in inhibiting lipoprotein lipase
 -catalyzed\nTG hydrolysis and attenuating receptor-mediated endocytosis of
 \nTG-rich lipoproteins\, several in vivo studies using stable isotopes\nha
 ve suggested a role of apoC-III in hepatic VLDL production in\nhumans. Our
  transfection experiments with cultured hepatic cells\nshowed that express
 ion of human apoC-III enhanced assembly and\nsecretion of apoB-100 in asso
 ciation with TAG-rich VLDL1 under\nlipid-rich conditions. Mutational analy
 sis with two naturally\noccurring human apoC-III mutants\, namely Ala23Thr
  and Lys58Glu\,\noriginally identified in respective hypotriglyceridemia a
 nd\nhyperalphalipoproteinemia subjects\, has revealed loss-of-function\nph
 enotype in VLDL1 assembly/secretion. Structural-functional\nanalysis has p
 rovided evidence for a two-domain model depicting\napoC-III action – the C
 -terminal lipid-binding domain (a typical\ntype A amphipathic a-helix) is 
 responsible for the formation of\nlumenal lipid droplets (LLD) that are a 
 precursor of VLDL1\, whereas\nthe N-terminal domain may play a role in pro
 moting fusion of LLD\nwith primordial VLDL. Kinetic studies have demonstra
 ted that\napoC-III\, working in tandem with MTP\, promotes formation of LL
 D.\nThe human apoC-III stimulated VLDL1-apoB-100 production was readily\no
 bserved (via adenovirus-mediated gene transfer) in apoC3-null mice\nfed wi
 th high fat diet or palm oil gavage. Further\, cells stably\nexpressing hu
 man apoC-III displayed resistance to ER stress (as\ndetermined by eIF2a ph
 osphorylation) induced by palmitic acid. The\ndata suggest that apoC-III m
 ay protect hepatic stress induced by\nlipotoxicity through purging lipids 
 as TG-rich VLDL1.\n\nMandatory for Graduate Students\n
DTSTART:20110414T200000Z
DTEND:20110414T200000Z
LOCATION:Life Sciences Complex\, CA\, QC\, Montreal\, H3G 0B1\, 3649 promen
 ade Sir William Osler
SUMMARY:Biochemistry Seminar Dr. Zemin Yao
URL:/channels/event/biochemistry-seminar-dr-zemin-yao-
 173399
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