Tags

Type your tag names separated by a space and hit enter

A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism.
Am J Physiol Endocrinol Metab 2007; 292(6):E1740-9AJ

Abstract

Fatty acid translocase (FAT)/CD36 is involved in regulating the uptake of long-chain fatty acids into muscle cells. However, the contribution of FAT/CD36 to fatty acid metabolism remains unknown. We examined the role of FAT/CD36 on fatty acid metabolism in perfused muscles (soleus and red and white gastrocnemius) of wild-type (WT) and FAT/CD36 null (KO) mice. In general, in muscles of KO mice, 1) insulin sensitivity and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) sensitivity were normal, 2) key enzymes involved in fatty acid oxidation were altered minimally or not at all, and 3) except for an increase in soleus muscle FATP1 and FATP4, these fatty acid transporters were not altered in red and white gastrocnemius muscles, whereas plasma membrane-bound fatty acid binding protein was not altered in any muscle. In KO muscles perfused under basal conditions (i.e., no insulin, no AICAR), rates of hindquarter fatty acid oxidation were reduced by 26%. Similarly, in oxidative but not glycolytic muscles, the basal rates of triacylglycerol esterification were reduced by 40%. When muscles were perfused with insulin, the net increase in fatty acid esterification was threefold greater in the oxidative muscles of WT mice compared with the oxidative muscles in KO mice. With AICAR-stimulation, the net increase in fatty acid oxidation by hindquarter muscles was 3.7-fold greater in WT compared with KO mice. In conclusion, the present studies demonstrate that FAT/CD36 has a critical role in regulating fatty acid esterification and oxidation, particularly during stimulation with insulin or AICAR.

Authors+Show Affiliations

Department of Human Health and Nutritional Science, University of Guelph, Guelph, Ontario, Canada N1G 2W1. abonen@uoguelph.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17264223

Citation

Bonen, Arend, et al. "A Null Mutation in Skeletal Muscle FAT/CD36 Reveals Its Essential Role in Insulin- and AICAR-stimulated Fatty Acid Metabolism." American Journal of Physiology. Endocrinology and Metabolism, vol. 292, no. 6, 2007, pp. E1740-9.
Bonen A, Han XX, Habets DD, et al. A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism. Am J Physiol Endocrinol Metab. 2007;292(6):E1740-9.
Bonen, A., Han, X. X., Habets, D. D., Febbraio, M., Glatz, J. F., & Luiken, J. J. (2007). A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism. American Journal of Physiology. Endocrinology and Metabolism, 292(6), pp. E1740-9.
Bonen A, et al. A Null Mutation in Skeletal Muscle FAT/CD36 Reveals Its Essential Role in Insulin- and AICAR-stimulated Fatty Acid Metabolism. Am J Physiol Endocrinol Metab. 2007;292(6):E1740-9. PubMed PMID: 17264223.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism. AU - Bonen,Arend, AU - Han,Xiao-Xia, AU - Habets,Daphna D J, AU - Febbraio,Maria, AU - Glatz,Jan F C, AU - Luiken,Joost J F P, Y1 - 2007/01/30/ PY - 2007/2/1/pubmed PY - 2007/7/31/medline PY - 2007/2/1/entrez SP - E1740 EP - 9 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 292 IS - 6 N2 - Fatty acid translocase (FAT)/CD36 is involved in regulating the uptake of long-chain fatty acids into muscle cells. However, the contribution of FAT/CD36 to fatty acid metabolism remains unknown. We examined the role of FAT/CD36 on fatty acid metabolism in perfused muscles (soleus and red and white gastrocnemius) of wild-type (WT) and FAT/CD36 null (KO) mice. In general, in muscles of KO mice, 1) insulin sensitivity and 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) sensitivity were normal, 2) key enzymes involved in fatty acid oxidation were altered minimally or not at all, and 3) except for an increase in soleus muscle FATP1 and FATP4, these fatty acid transporters were not altered in red and white gastrocnemius muscles, whereas plasma membrane-bound fatty acid binding protein was not altered in any muscle. In KO muscles perfused under basal conditions (i.e., no insulin, no AICAR), rates of hindquarter fatty acid oxidation were reduced by 26%. Similarly, in oxidative but not glycolytic muscles, the basal rates of triacylglycerol esterification were reduced by 40%. When muscles were perfused with insulin, the net increase in fatty acid esterification was threefold greater in the oxidative muscles of WT mice compared with the oxidative muscles in KO mice. With AICAR-stimulation, the net increase in fatty acid oxidation by hindquarter muscles was 3.7-fold greater in WT compared with KO mice. In conclusion, the present studies demonstrate that FAT/CD36 has a critical role in regulating fatty acid esterification and oxidation, particularly during stimulation with insulin or AICAR. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/17264223/A_null_mutation_in_skeletal_muscle_FAT/CD36_reveals_its_essential_role_in_insulin__and_AICAR_stimulated_fatty_acid_metabolism_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00579.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -