title: Retinoic acid treatment increases lipid oxidation capacity in skeletal muscle of mice.
abstract: OBJECTIVE
  All-trans retinoic acid (ATRA), a carboxylic form of vitamin A, favors in mice a mobilization of body fat reserves that correlates with an increment of oxidative and thermogenic capacity in adipose tissues. The objective of this study has been to investigate the effect of ATRA treatment on skeletal muscle capacity for fatty-acid catabolism.
  
  
  METHODS
  Tissue composition and gene expression related to lipid and oxidative metabolism were analyzed in skeletal muscle of mice acutely treated with ATRA or vehicle (olive oil).
  
  
  RESULTS
  ATRA treatment triggered a dose-dependent increase in the muscle mRNA expression levels of selected enzymes, transporters and transcription factors involved in fatty-acid oxidation, respiration, and thermogenesis namely: muscle-type carnitine palmitoyltransferase 1, acyl CoA oxidase 1, subunit II of cytochrome oxidase, uncoupling protein 3, peroxisome proliferator-activated receptor-gamma co-activator -1alpha and peroxisome proliferator-activated receptor-delta (PPARdelta). The treatment also resulted in the upregulation of the mRNA levels of acetyl-CoA carboxylase 2 (ACC2), a key regulatory enzyme for mitochondrial fatty-acid oxidation in muscle. Skeletal muscle protein levels of PPARdelta and retinoid X receptor gamma, a partner for many nuclear receptors involved in lipid metabolism, were increased after ATRA treatment. Muscle lipid content was decreased.
  
  
  CONCLUSIONS
  These results indicate that ATRA treatment increases the capacity of skeletal muscle for fatty-acid oxidation. Knowledge of nutrients or nutrient-derivatives capable of enhancing oxidative metabolism in muscle and other tissues can contribute to new avenues of prevention and treatment of obesity and related disorders.
authors.affiliation: Laboratory of Molecular Biology, Nutrition and Biotechnology, Universitat de les Illes Balears, Palma de Mallorca, Spain.
authors.forename: Jaume
authors.initials: J
authors.lastname: Amengual
authors.forename: Joan
authors.initials: J
authors.lastname: Ribot
authors.forename: M Luisa
authors.initials: ML
authors.lastname: Bonet
authors.forename: Andreu
authors.initials: A
authors.lastname: Palou
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D042962:Acyl-CoA Oxidase / Q000378:metabolism; D000818:Animals; D019440:Anti-Obesity Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects; D005227:Fatty Acids / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D007279:Injections, Subcutaneous; D050356:Lipid Metabolism / Q000187:drug effects / Q000235:genetics; D008297:Male; D051379:Mice; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D010084:Oxidation-Reduction; D047495:PPAR gamma / Q000378:metabolism; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012333:RNA, Messenger / Q000378:metabolism; D047491:Retinoid X Receptor gamma / Q000378:metabolism; D015534:Trans-Activators / Q000378:metabolism; D014157:Transcription Factors; D014212:Tretinoin / Q000008:administration & dosage / Q000494:pharmacology*; D014280:Triglycerides / Q000378:metabolism
chemical_list: D019440:Anti-Obesity Agents; D005227:Fatty Acids; D047495:PPAR gamma; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C485290:Ppargc1a protein, mouse; D012333:RNA, Messenger; D047491:Retinoid X Receptor gamma; D015534:Trans-Activators; D014157:Transcription Factors; D014280:Triglycerides; D014212:Tretinoin; D042962:Acyl-CoA Oxidase; C117108:cytochrome C oxidase subunit II; D003576:Electron Transport Complex IV; D002334:Carnitine O-Palmitoyltransferase; C498191:Acacb protein, mouse; D000103:Acetyl-CoA Carboxylase