Endocrine control of oleic acid and glucose metabolism in rainbow trout (Oncorhynchus mykiss) muscle cells in culture.
The effects of insulin and IGF-I on fatty acid (FA) and glucose metabolism were examined using oleic acid or glucose as tracers in differentiated rainbow trout (Oncorhynchus mykiss) myotubes. Insulin and IGF-I significantly reduced the production of CO(2) from oleic acid with respect to the control values. IGF-I also significantly reduced the production of acid-soluble products (ASP) and the concentration of FA in the medium, while cellular triacylglycerols (TAG) tended to increase. Only insulin produced a significant accumulation of glycogen inside the cells in glucose distribution experiments. Incubation with catecholamines did not affect oleic acid metabolism. Cells treated with rapamycin [a target of rapamycin (TOR) inhibitor] significantly increased the oxidation of oleic acid to CO(2) and ASP, while the accumulation of TAG diminished. Rosiglitazone (a peroxisome proliferator-activated receptor gamma agonist) and etomoxir (a CPT-1 inhibitor) produced a severe and significant reduction in the production of CO(2) and ASP. Rosiglitazone and etomoxir also produced a significant accumulation of FA outside and inside the cells, respectively. No significant effects of these drugs on glucose distribution were observed. These data indicate that insulin and IGF-I act as anabolic hormones in trout myotubes in both oleic acid and glucose metabolism, although glucose oxidation appears to be less sensitive than FA oxidation to insulin and IGF-I. The use of rapamycin, etomoxir, and rosiglitazone may help us to understand the mechanisms of regulation of lipid metabolism in fish.
Sánchez-Gurmaches
Joan
J
Dept. de Fisiologia, Facultat de Biologia, Universitat de Barcelona, Catalunya, Spain. juansangu@gmail.com
Cruz-Garcia
Lourdes
L
Gutiérrez
Joaquím
J
Navarro
Isabel
I
D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002334:Carnitine O-Palmitoyltransferase / Q000037:antagonists & inhibitors / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D002478:Cells, Cultured; D004734:Energy Metabolism / Q000187:drug effects; D004852:Epoxy Compounds / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D047908:Intracellular Signaling Peptides and Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism*; D019301:Oleic Acid / Q000378:metabolism*; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D010084:Oxidation-Reduction; D047495:PPAR gamma / Q000819:agonists / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D000077154:Rosiglitazone; D020123:Sirolimus / Q000494:pharmacology; D058570:TOR Serine-Threonine Kinases; D045162:Thiazolidinediones / Q000494:pharmacology; D014280:Triglycerides / Q000378:metabolism
D002395:Catecholamines; D004852:Epoxy Compounds; D007004:Hypoglycemic Agents; D007328:Insulin; D047908:Intracellular Signaling Peptides and Proteins; D047495:PPAR gamma; D047428:Protein Kinase Inhibitors; D045162:Thiazolidinediones; D014280:Triglycerides; D000077154:Rosiglitazone; D002245:Carbon Dioxide; D019301:Oleic Acid; D007334:Insulin-Like Growth Factor I; D006003:Glycogen; D002334:Carnitine O-Palmitoyltransferase; D017346:Protein Serine-Threonine Kinases; D058570:TOR Serine-Threonine Kinases; D005947:Glucose; C054207:etomoxir; D020123:Sirolimus