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Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36.
FASEB J 2004; 18(10):1144-6FJ

Abstract

We examined whether, in human obesity and type 2 diabetes, long chain fatty acid (LCFA) transport into skeletal muscle is upregulated and contributes to an excess intramuscular triacylglycerol accumulation. In giant sarcolemmal vesicles prepared from human skeletal muscle, LCFA transport rates were upregulated approximately 4-fold and were associated with an increased intramuscular triacylglycerol content in obese individuals and in type 2 diabetics. In these individuals, the increased sarcolemmal LCFA transport rate was not associated with an altered expression of FAT/CD36 or FABPpm. Instead, the increase in the LCFA transport rate was associated with an increase in sarcolemmal FAT/CD36 but not sarcolemmal FABPpm. Rates of fatty acid esterification were increased threefold in isolated human muscle strips obtained from obese subjects, while concomitantly rates of fatty acid oxidation were not altered. Thus, the increased rate of fatty acid transport may contribute to the increased rates of triacylglycerol accumulation in human skeletal muscle. The altered FAT/CD36 trafficking in muscle from obese subjects and type 2 diabetics juxtaposes the known alterations in GLUT4 trafficking, i.e., GLUT4 is known to be retained in its intracellular depots while FAT/CD36 is retained at the sarcolemma. This redistribution of FAT/CD36 to the sarcolemma may contribute to the etiology of insulin resistance in human muscle, and hence, FAT/CD36 provides another potential therapeutic target for the prevention and/or treatment of insulin resistance.

Authors+Show Affiliations

Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, N1G 2W1, Canada. abonen@uogulph.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15132977

Citation

Bonen, Arend, et al. "Triacylglycerol Accumulation in Human Obesity and Type 2 Diabetes Is Associated With Increased Rates of Skeletal Muscle Fatty Acid Transport and Increased Sarcolemmal FAT/CD36." FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, vol. 18, no. 10, 2004, pp. 1144-6.
Bonen A, Parolin ML, Steinberg GR, et al. Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36. FASEB J. 2004;18(10):1144-6.
Bonen, A., Parolin, M. L., Steinberg, G. R., Calles-Escandon, J., Tandon, N. N., Glatz, J. F., ... Dyck, D. J. (2004). Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 18(10), pp. 1144-6.
Bonen A, et al. Triacylglycerol Accumulation in Human Obesity and Type 2 Diabetes Is Associated With Increased Rates of Skeletal Muscle Fatty Acid Transport and Increased Sarcolemmal FAT/CD36. FASEB J. 2004;18(10):1144-6. PubMed PMID: 15132977.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36. AU - Bonen,Arend, AU - Parolin,Michelle L, AU - Steinberg,Gregory R, AU - Calles-Escandon,Jorge, AU - Tandon,Narendra N, AU - Glatz,Jan F C, AU - Luiken,Joost J F P, AU - Heigenhauser,George J F, AU - Dyck,David J, Y1 - 2004/05/07/ PY - 2004/5/11/pubmed PY - 2005/1/6/medline PY - 2004/5/11/entrez SP - 1144 EP - 6 JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology JO - FASEB J. VL - 18 IS - 10 N2 - We examined whether, in human obesity and type 2 diabetes, long chain fatty acid (LCFA) transport into skeletal muscle is upregulated and contributes to an excess intramuscular triacylglycerol accumulation. In giant sarcolemmal vesicles prepared from human skeletal muscle, LCFA transport rates were upregulated approximately 4-fold and were associated with an increased intramuscular triacylglycerol content in obese individuals and in type 2 diabetics. In these individuals, the increased sarcolemmal LCFA transport rate was not associated with an altered expression of FAT/CD36 or FABPpm. Instead, the increase in the LCFA transport rate was associated with an increase in sarcolemmal FAT/CD36 but not sarcolemmal FABPpm. Rates of fatty acid esterification were increased threefold in isolated human muscle strips obtained from obese subjects, while concomitantly rates of fatty acid oxidation were not altered. Thus, the increased rate of fatty acid transport may contribute to the increased rates of triacylglycerol accumulation in human skeletal muscle. The altered FAT/CD36 trafficking in muscle from obese subjects and type 2 diabetics juxtaposes the known alterations in GLUT4 trafficking, i.e., GLUT4 is known to be retained in its intracellular depots while FAT/CD36 is retained at the sarcolemma. This redistribution of FAT/CD36 to the sarcolemma may contribute to the etiology of insulin resistance in human muscle, and hence, FAT/CD36 provides another potential therapeutic target for the prevention and/or treatment of insulin resistance. SN - 1530-6860 UR - https://www.unboundmedicine.com/medline/citation/15132977/Triacylglycerol_accumulation_in_human_obesity_and_type_2_diabetes_is_associated_with_increased_rates_of_skeletal_muscle_fatty_acid_transport_and_increased_sarcolemmal_FAT/CD36_ L2 - http://www.fasebj.org/doi/full/10.1096/fj.03-1065fje?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -