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...

Full description

Bibliographic Details
Main Authors: Arend Bonen, Xiao-Xia Han, Narendra N. Tandon, Jan F.C. Glatz, James Lally, Laelie A. Snook, Joost J. F.P. Luiken
Format: Article
Language:English
Published: Elsevier 2009-04-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520308725
id doaj-63781b0538d545c0aac19a006c3b8342
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
_version_ 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