Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

McFarlan 2012 J Biol Chem

From Bioblast
Publications in the MiPMap
McFarlan JT, Yoshida Y, Jain SS, Han XX, Snook LA, Lally J, Smith BK, Glatz JF, Luiken JJ, Sayer RA, Tupling AR, Chabowski A, Holloway GP, Bonen A (2012) In vivo, fatty acid translocase (CD36) critically regulates skeletal muscle fuel selection, exercise performance and training-induced adaptation of fatty acid oxidation. J Biol Chem 287:23502-16.

Β» PMID: 22584574 Open Access

McFarlan JT, Yoshida Y, Jain SS, Han XX, Snook LA, Lally J, Smith BK, Glatz JF, Luiken JJ, Sayer RA, Tupling AR, Chabowski A, Holloway GP, Bonen A (2012) J Biol Chem

Abstract: For ~40 years it has been widely accepted that i) the exercise-induced increase in muscle fatty acid oxidation (FAO) is dependent on the increased delivery of circulating fatty acids, and ii) exercise-training-induced FAO upregulation is largely attributable to muscle mitochondrial biogenesis. These long-standing concepts were developed prior to recent recognition that fatty acid entry into muscle occurs via a regulatable, sarcolemmal CD36-mediated mechanism. We examined the role of CD36 in muscle fuel selection under basal conditions, during a metabolic challenge (exercise), and after exercise-training. We also investigated whether CD36 overexpression, independent of mitochondrial changes, mimicked exercise-training-induced FAO upregulation. Under basal conditions CD36-KO vs WT mice displayed reduced fatty acid transport (-21%) and oxidation (-25%), intramuscular lipids (<-31%), and hepatic glycogen (-20%); but muscle glycogen, VO2max, and mitochondrial content and enzymes did not differ. In acutely exercised (78%VO2max) CD36-KO mice, fatty acid transport (-41%) and oxidation (-37%), and exercise duration (-44%) were reduced, while muscle and hepatic glycogen depletions were accelerated by 27-55%, revealing 2-fold greater carbohydrate use. Exercise-training increased mtDNA and Ξ²-HAD similarly in WT and CD36-KO muscles, but FAO was increased only in WT muscle (+90%). Comparable CD36 increases, induced by exercise-training (+44%) or by CD36-overexpression (+41%), increased FAO similarly (84-90%), either when mitochondrial biogenesis and FAO enzymes were upregulated (exercise-training) or when these were unaltered (CD36-overexpression). Thus, sarcolemmal CD36 has a key role in muscle fuel selection, exercise performance and training-induced muscle FAO adaptation, challenging long-held, views of mechanisms involved in acute and adaptive regulation of muscle FAO. β€’ Keywords: CD36-KO mice, Fatty acids, Transport, Exercise, Training, Muscle, Transfection

β€’ O2k-Network Lab: CA Guelph Holloway GP


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mtDNA;mt-genetics, Exercise physiology;nutrition;life style 


Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Regulation: Fatty acid 


HRR: Oxygraph-2k