FAT/CD36 expression is not ablated in spontaneously hypertensive rats
There is doubt whether spontaneously hypertensive rats (SHR; North American strain) are null for fatty acid translocase (FAT/CD36). Therefore, we examined whether FAT/CD36 is expressed in heart, muscle, liver and adipose tissue in SHR. Insulin resistance was present in SHR skeletal muscle. We confir...
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Format: | Article |
Language: | English |
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Elsevier
2009-04-01
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Series: | Journal of Lipid Research |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520308725 |
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doaj-63781b0538d545c0aac19a006c3b8342 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Arend Bonen Xiao-Xia Han Narendra N. Tandon Jan F.C. Glatz James Lally Laelie A. Snook Joost J. F.P. Luiken |
spellingShingle |
Arend Bonen Xiao-Xia Han Narendra N. Tandon Jan F.C. Glatz James Lally Laelie A. Snook Joost J. F.P. Luiken FAT/CD36 expression is not ablated in spontaneously hypertensive rats Journal of Lipid Research muscle heart liver adipose tissue glucose transport fatty acid transport |
author_facet |
Arend Bonen Xiao-Xia Han Narendra N. Tandon Jan F.C. Glatz James Lally Laelie A. Snook Joost J. F.P. Luiken |
author_sort |
Arend Bonen |
title |
FAT/CD36 expression is not ablated in spontaneously hypertensive rats |
title_short |
FAT/CD36 expression is not ablated in spontaneously hypertensive rats |
title_full |
FAT/CD36 expression is not ablated in spontaneously hypertensive rats |
title_fullStr |
FAT/CD36 expression is not ablated in spontaneously hypertensive rats |
title_full_unstemmed |
FAT/CD36 expression is not ablated in spontaneously hypertensive rats |
title_sort |
fat/cd36 expression is not ablated in spontaneously hypertensive rats |
publisher |
Elsevier |
series |
Journal of Lipid Research |
issn |
0022-2275 |
publishDate |
2009-04-01 |
description |
There is doubt whether spontaneously hypertensive rats (SHR; North American strain) are null for fatty acid translocase (FAT/CD36). Therefore, we examined whether FAT/CD36 is expressed in heart, muscle, liver and adipose tissue in SHR. Insulin resistance was present in SHR skeletal muscle. We confirmed that SHR expressed aberrant FAT mRNAs in key metabolic tissues; namely, the major 2.9 kb transcript was not expressed, but 3.8 and 5.4 kb transcripts were present. Despite this, FAT/CD36 protein was expressed in all tissues, although there were tissue-specific reductions in FAT/CD36 protein expression and plasmalemmal content, ranging from 26–85%. Fatty acid transport was reduced in adipose tissue (−50%) and was increased in liver (+47%). Normal rates of fatty acid transport occurred in heart and muscle, possibly due to compensatory upregulation of plasmalemmal fatty acid binding protein (FABPpm) in red (+123%) and white muscle (+110%). In conclusion, SHRs (North American strain) are not a natural FAT/CD36 null model, the North American strain of SHR express FAT/CD36, albeit at reduced levels. |
topic |
muscle heart liver adipose tissue glucose transport fatty acid transport |
url |
http://www.sciencedirect.com/science/article/pii/S0022227520308725 |
work_keys_str_mv |
AT arendbonen fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT xiaoxiahan fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT narendrantandon fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT janfcglatz fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT jameslally fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT laelieasnook fatcd36expressionisnotablatedinspontaneouslyhypertensiverats AT joostjfpluiken fatcd36expressionisnotablatedinspontaneouslyhypertensiverats |
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1721504839929692160 |
spelling |
doaj-63781b0538d545c0aac19a006c3b83422021-04-28T05:57:08ZengElsevierJournal of Lipid Research0022-22752009-04-01504740748FAT/CD36 expression is not ablated in spontaneously hypertensive ratsArend Bonen0Xiao-Xia Han1Narendra N. Tandon2Jan F.C. Glatz3James Lally4Laelie A. Snook5Joost J. F.P. Luiken6Department of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsDepartment of Human Health and Nutritional Sciences University of -Guelph, Guelph, Ontario, N1G 2W1, Canada; Thrombosis Research Laboratory, Otsuka Maryland Medicinal Laboratories 9900 Medical Center Drive, Rockville, MD 20850, Maastricht University, 6200-MD Maastricht, The Netherlands; Department of Molecular Genetics, Maastricht University, 6200-MD Maastricht, The NetherlandsThere is doubt whether spontaneously hypertensive rats (SHR; North American strain) are null for fatty acid translocase (FAT/CD36). Therefore, we examined whether FAT/CD36 is expressed in heart, muscle, liver and adipose tissue in SHR. Insulin resistance was present in SHR skeletal muscle. We confirmed that SHR expressed aberrant FAT mRNAs in key metabolic tissues; namely, the major 2.9 kb transcript was not expressed, but 3.8 and 5.4 kb transcripts were present. Despite this, FAT/CD36 protein was expressed in all tissues, although there were tissue-specific reductions in FAT/CD36 protein expression and plasmalemmal content, ranging from 26–85%. Fatty acid transport was reduced in adipose tissue (−50%) and was increased in liver (+47%). Normal rates of fatty acid transport occurred in heart and muscle, possibly due to compensatory upregulation of plasmalemmal fatty acid binding protein (FABPpm) in red (+123%) and white muscle (+110%). In conclusion, SHRs (North American strain) are not a natural FAT/CD36 null model, the North American strain of SHR express FAT/CD36, albeit at reduced levels.http://www.sciencedirect.com/science/article/pii/S0022227520308725muscleheartliver adiposetissueglucose transportfatty acid transport |