Targeted Deletion of Hepatocyte ABCA1 Leads to Very Low Density Lipoprotein Triglyceride Overproduction and Low Density Lipoprotein Hypercatabolism
Loss of ABCA1 activity in Tangier disease (TD) is associated with abnormal apoB lipoprotein (Lp) metabolism in addition to the complete absence of high density lipoprotein (HDL). We used hepatocyte-specific ABCA1 knock-out (HSKO) mice to test the hypothesis that hepatic ABCA1 plays dual roles in reg...
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Published in | The Journal of biological chemistry Vol. 285; no. 16; pp. 12197 - 12209 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
16.04.2010
American Society for Biochemistry and Molecular Biology |
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Abstract | Loss of ABCA1 activity in Tangier disease (TD) is associated with abnormal apoB lipoprotein (Lp) metabolism in addition to the complete absence of high density lipoprotein (HDL). We used hepatocyte-specific ABCA1 knock-out (HSKO) mice to test the hypothesis that hepatic ABCA1 plays dual roles in regulating Lp metabolism and nascent HDL formation. HSKO mice recapitulated the TD lipid phenotype with postprandial hypertriglyceridemia, markedly decreased LDL, and near absence of HDL. Triglyceride (TG) secretion was 2-fold higher in HSKO compared with wild type mice, primarily due to secretion of larger TG-enriched VLDL secondary to reduced hepatic phosphatidylinositol 3-kinase signaling. HSKO mice also displayed delayed clearance of postprandial TG and reduced post-heparin plasma lipolytic activity. In addition, hepatic LDLr expression and plasma LDL catabolism were increased 2-fold in HSKO compared with wild type mice. Last, adenoviral repletion of hepatic ABCA1 in HSKO mice normalized plasma VLDL TG and hepatic phosphatidylinositol 3-kinase signaling, with a partial recovery of HDL cholesterol levels, providing evidence that hepatic ABCA1 is involved in the reciprocal regulation of apoB Lp production and HDL formation. These findings suggest that altered apoB Lp metabolism in TD subjects may result from hepatic VLDL TG overproduction and increased hepatic LDLr expression and highlight hepatic ABCA1 as an important regulatory factor for apoB-containing Lp metabolism. |
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AbstractList | Loss of ABCA1 activity in Tangier disease (TD) is associated with abnormal apoB lipoprotein (Lp) metabolism in addition to the complete absence of high density lipoprotein (HDL). We used hepatocyte-specific ABCA1 knock-out (HSKO) mice to test the hypothesis that hepatic ABCA1 plays dual roles in regulating Lp metabolism and nascent HDL formation. HSKO mice recapitulated the TD lipid phenotype with postprandial hypertriglyceridemia, markedly decreased LDL, and near absence of HDL. Triglyceride (TG) secretion was 2-fold higher in HSKO compared with wild type mice, primarily due to secretion of larger TG-enriched VLDL secondary to reduced hepatic phosphatidylinositol 3-kinase signaling. HSKO mice also displayed delayed clearance of postprandial TG and reduced post-heparin plasma lipolytic activity. In addition, hepatic LDLr expression and plasma LDL catabolism were increased 2-fold in HSKO compared with wild type mice. Last, adenoviral repletion of hepatic ABCA1 in HSKO mice normalized plasma VLDL TG and hepatic phosphatidylinositol 3-kinase signaling, with a partial recovery of HDL cholesterol levels, providing evidence that hepatic ABCA1 is involved in the reciprocal regulation of apoB Lp production and HDL formation. These findings suggest that altered apoB Lp metabolism in TD subjects may result from hepatic VLDL TG overproduction and increased hepatic LDLr expression and highlight hepatic ABCA1 as an important regulatory factor for apoB-containing Lp metabolism. |
Author | Chung, Soonkyu Duong, MyNgan Hayden, Michael R. Sawyer, Janet K. Shelness, Gregory S. Parks, John S. Timmins, Jenelle M. Rong, Shunxing Rudel, Lawrence L. Singaraja, Roshni R. Degirolamo, Chiara Maeda, Nobuyo |
Author_xml | – sequence: 1 givenname: Soonkyu surname: Chung fullname: Chung, Soonkyu organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 2 givenname: Jenelle M. surname: Timmins fullname: Timmins, Jenelle M. organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 3 givenname: MyNgan surname: Duong fullname: Duong, MyNgan organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 4 givenname: Chiara surname: Degirolamo fullname: Degirolamo, Chiara organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 5 givenname: Shunxing surname: Rong fullname: Rong, Shunxing organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 6 givenname: Janet K. surname: Sawyer fullname: Sawyer, Janet K. organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 7 givenname: Roshni R. surname: Singaraja fullname: Singaraja, Roshni R. organization: Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada – sequence: 8 givenname: Michael R. surname: Hayden fullname: Hayden, Michael R. organization: Centre for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, British Columbia V5Z 4H4, Canada – sequence: 9 givenname: Nobuyo surname: Maeda fullname: Maeda, Nobuyo organization: Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina 27599 – sequence: 10 givenname: Lawrence L. surname: Rudel fullname: Rudel, Lawrence L. organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 11 givenname: Gregory S. surname: Shelness fullname: Shelness, Gregory S. organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 – sequence: 12 givenname: John S. surname: Parks fullname: Parks, John S. email: jparks@wfubmc.edu organization: Department of Pathology/Section on Lipid Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina 27157 |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20178985$$D View this record in MEDLINE/PubMed |
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Keywords | Low Density Lipoprotein (LDL) Lipoprotein Very Low Density Lipoprotein (VLDL) Hepatocyte PI 3-Kinase ABC Transporter |
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SubjectTerms | ABC Transporter Adenoviridae - genetics Animals Apolipoproteins B - metabolism ATP Binding Cassette Transporter 1 ATP-Binding Cassette Transporters - antagonists & inhibitors ATP-Binding Cassette Transporters - genetics ATP-Binding Cassette Transporters - metabolism Disease Models, Animal Gene Expression Gene Targeting Hepatocyte Hepatocytes - metabolism Humans Hypertriglyceridemia - genetics Hypertriglyceridemia - metabolism Lipids Lipoprotein Lipoproteins, HDL - biosynthesis Lipoproteins, LDL - metabolism Lipoproteins, VLDL - biosynthesis Low Density Lipoprotein (LDL) Male Metabolism Mice Mice, Inbred C57BL Mice, Knockout Phosphatidylinositol 3-Kinases - metabolism PI 3-Kinase Recombinant Proteins - genetics Recombinant Proteins - metabolism Tangier Disease - genetics Tangier Disease - metabolism Triglycerides - biosynthesis Very Low Density Lipoprotein (VLDL) |
Title | Targeted Deletion of Hepatocyte ABCA1 Leads to Very Low Density Lipoprotein Triglyceride Overproduction and Low Density Lipoprotein Hypercatabolism |
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