Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings
LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the hi...
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| Format: | Article |
| Language: | English |
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Elsevier
2020-08-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520434832 |
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doaj-1eb59149604d406ab618b04f2a2cf3f0 |
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Article |
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DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Kaare R. Norum Alan T. Remaley Helena E. Miettinen Erik H. Strøm Bruno E.P. Balbo Carlos A.T.L. Sampaio Ingrid Wiig Jan Albert Kuivenhoven Laura Calabresi John J. Tesmer Mingyue Zhou Dominic S. Ng Bjørn Skeie Sotirios K. Karathanasis Kelly A. Manthei Kjetil Retterstøl |
| spellingShingle |
Kaare R. Norum Alan T. Remaley Helena E. Miettinen Erik H. Strøm Bruno E.P. Balbo Carlos A.T.L. Sampaio Ingrid Wiig Jan Albert Kuivenhoven Laura Calabresi John J. Tesmer Mingyue Zhou Dominic S. Ng Bjørn Skeie Sotirios K. Karathanasis Kelly A. Manthei Kjetil Retterstøl Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings Journal of Lipid Research HDL cholesterol lipoprotein cardiovascular heart disease lipoprotein X |
| author_facet |
Kaare R. Norum Alan T. Remaley Helena E. Miettinen Erik H. Strøm Bruno E.P. Balbo Carlos A.T.L. Sampaio Ingrid Wiig Jan Albert Kuivenhoven Laura Calabresi John J. Tesmer Mingyue Zhou Dominic S. Ng Bjørn Skeie Sotirios K. Karathanasis Kelly A. Manthei Kjetil Retterstøl |
| author_sort |
Kaare R. Norum |
| title |
Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| title_short |
Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| title_full |
Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| title_fullStr |
Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| title_full_unstemmed |
Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| title_sort |
lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings |
| publisher |
Elsevier |
| series |
Journal of Lipid Research |
| issn |
0022-2275 |
| publishDate |
2020-08-01 |
| description |
LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD. |
| topic |
HDL cholesterol lipoprotein cardiovascular heart disease lipoprotein X |
| url |
http://www.sciencedirect.com/science/article/pii/S0022227520434832 |
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doaj-1eb59149604d406ab618b04f2a2cf3f02021-04-29T04:38:41ZengElsevierJournal of Lipid Research0022-22752020-08-0161811421149Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findingsKaare R. Norum0Alan T. Remaley1Helena E. Miettinen2Erik H. Strøm3Bruno E.P. Balbo4Carlos A.T.L. Sampaio5Ingrid Wiig6Jan Albert Kuivenhoven7Laura Calabresi8John J. Tesmer9Mingyue Zhou10Dominic S. Ng11Bjørn Skeie12Sotirios K. Karathanasis13Kelly A. Manthei14Kjetil Retterstøl15Department of Nutrition, University of Oslo, Oslo, NorwayTo whom correspondence should be addressed: (A.T.R.) alan.remaley@nih.gov; National Institutes of Health, Bethesda, MD; To whom correspondence should be addressed: (K.R.) kjetil.retterstol@medisin.uio.noDepartment of Medicine, University of Helsinki and University Central Hospital, Helsinki, FinlandDepartments of Pathology Oslo University Hospital, Oslo, NorwayDivision of Nephrology and Molecular Medicine Department of Medicine, University of São Paulo School of Medicine, São Paulo, BrazilDivision of Nephrology and Molecular Medicine Department of Medicine, University of São Paulo School of Medicine, São Paulo, BrazilCentre for Rare Disorders, Oslo University Hospital, Oslo, NorwayDepartment of Pediatrics, Section Molecular Genetics, University Medical Center Groningen, University of Groningen, Groningen, The NetherlandsCenter E. Grossi Paoletti, Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, ItalyDepartment of Biological Sciences, Purdue University, West Lafayette, INCardiometabolic Disorder Research, AMGEN, San Francisco, CADepartment of Medicine, University of Toronto and Keenan Research Center, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, CanadaAnesthesiology, Oslo University Hospital, Oslo, NorwayTo whom correspondence should be addressed: (S.K.K.) sotirios.karathanasis@nih.gov; National Institutes of Health, Bethesda, MD; Department of NeoProgen, Baltimore, MD; To whom correspondence should be addressed: (K.R.) kjetil.retterstol@medisin.uio.noTo whom correspondence should be addressed: (K.A.M.) kmanthei@umich.edu; Life Sciences Institute, University of Michigan, Ann Arbor, MI; To whom correspondence should be addressed: (K.R.) kjetil.retterstol@medisin.uio.noTo whom correspondence should be addressed: (K.R.) kjetil.retterstol@medisin.uio.no; Department of Nutrition, University of Oslo, Oslo, Norway; Department of Endocrinology, Morbid Obesity, and Preventive Medicine, Lipid Clinic, Oslo University Hospital, Oslo, Norway; To whom correspondence should be addressed: (K.R.) kjetil.retterstol@medisin.uio.noLCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD.http://www.sciencedirect.com/science/article/pii/S0022227520434832HDL cholesterollipoproteincardiovascular heart diseaselipoprotein X |