Nutritional regulation and role of peroxisome proliferator-activated receptor delta in fatty acid catabolism in skeletal muscle
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Nutritional regulation and role of peroxisome proliferator-activated receptor delta in fatty acid catabolism in skeletal muscle. / Holst, Dorte; Luquet, Serge; Nogueira, Véronique; Kristiansen, Karsten; Leverve, Xavier; Grimaldi, Paul A.
In: BBA General Subjects, Vol. 1633, No. 1, 04.07.2003, p. 43-50.Research output: Contribution to journal › Journal article › peer-review
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TY - JOUR
T1 - Nutritional regulation and role of peroxisome proliferator-activated receptor delta in fatty acid catabolism in skeletal muscle
AU - Holst, Dorte
AU - Luquet, Serge
AU - Nogueira, Véronique
AU - Kristiansen, Karsten
AU - Leverve, Xavier
AU - Grimaldi, Paul A
PY - 2003/7/4
Y1 - 2003/7/4
N2 - Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARdelta displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARdelta mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARdelta is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARdelta in muscle cells, we forced its expression and that of a dominant-negative PPARdelta mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARdelta agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARdelta enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. These data strongly support a role for PPARdelta in the regulation of fatty acid oxidation in skeletal muscle and in adaptive response of this tissue to lipid catabolism.
AB - Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors primarily involved in lipid homeostasis. PPARdelta displays strong expression in tissues with high lipid metabolism, such as adipose, intestine and muscle. Its role in skeletal muscle remains largely unknown. After a 24-h starvation period, PPARdelta mRNA levels are dramatically up-regulated in gastrocnemius muscle of mice and restored to control level upon refeeding. The rise of PPARdelta is accompanied by parallel up-regulations of fatty acid translocase/CD36 (FAT/CD36) and heart fatty acid binding protein (H-FABP), while refeeding promotes down-regulation of both genes. To directly access the role of PPARdelta in muscle cells, we forced its expression and that of a dominant-negative PPARdelta mutant in C2C12 myogenic cells. Differentiated C2C12 cells responds to 2-bromopalmitate or synthetic PPARdelta agonist by induction of genes involved in lipid metabolism and increment of fatty acid oxidation. Overexpression of PPARdelta enhanced these cellular responses, whereas expression of the dominant-negative mutant exerts opposite effects. These data strongly support a role for PPARdelta in the regulation of fatty acid oxidation in skeletal muscle and in adaptive response of this tissue to lipid catabolism.
KW - Animals
KW - Carbon Radioisotopes
KW - Cell Differentiation
KW - Cell Line
KW - Fatty Acids
KW - Gene Expression Regulation
KW - Kinetics
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Muscle, Skeletal
KW - Mutation
KW - Nutritional Physiological Phenomena
KW - Palmitates
KW - RNA, Messenger
KW - Receptors, Cytoplasmic and Nuclear
KW - Transcription Factors
KW - Transcriptional Activation
M3 - Journal article
C2 - 12842194
VL - 1633
SP - 43
EP - 50
JO - B B A - General Subjects
JF - B B A - General Subjects
SN - 0304-4165
IS - 1
ER -
ID: 35457582