Rainbow trout genetically selected for greater muscle fat content display increased activation of liver TOR signaling and lipogenic gene expression.
Genetic selection is commonly used in farm animals to manage body fat content. In rainbow trout, divergent selection for low or high muscle fat content leads to differences in utilization of dietary energy sources between the fat muscle line (FL) and the lean muscle line (LL). To establish whether genetic selection on muscle fat content affects the hepatic insulin/nutrient signaling pathway, we analyzed this pathway and the expression of several metabolism-related target genes in the livers of the two divergent lines under fasting and then refeeding conditions. Whereas glycemia returned to basal level 24 h after refeeding in FL trout, it remained elevated in the LL trout. Target of rapamycin (TOR) protein was more abundant in the livers of FL trout than in LL trout, and refeeding activation of the hepatic TOR signaling pathway (TOR, S6K1, and S6) was therefore enhanced. Genes related to glycolysis (glucokinase and pyruvate kinase) and gluconeogenesis (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) were only slightly affected by refeeding and genetic selection. Refeeding stimulated expression of lipogenic genes and the sterol-responsive element binding protein (SREBP1), and expression of fatty acid synthase, glucose-6-phosphate dehydrogenase, and serine dehydratase was predominant in the livers of FL fish compared with LL fish. In agreement with recent findings linking TOR to lipogenesis control, we concluded that genetic selection for muscle fat content resulted in overactivation of the TOR signaling pathway-associated lipogenesis and probably also improved utilization of glucose.
Skiba-Cassy
Sandrine
S
Unité Mixte de Recherches 1067 Nutrition Aquaculture and Génomique, Institut National de la Recherche Agronomique, Pôle d'hydrobiologie, 64310 Saint Pée-sur-Nivelle, France. skiba@st-pee.inra.fr
Lansard
Marine
M
Panserat
Stéphane
S
Médale
Françoise
F
D000818:Animals; D001823:Body Composition / Q000235:genetics / Q000502:physiology; D001835:Body Weight / Q000235:genetics / Q000502:physiology; D064429:Fatty Acid Synthases; D005954:Glucosephosphate Dehydrogenase; D007328:Insulin / Q000235:genetics / Q000378:metabolism; D012695:L-Serine Dehydratase; D050356:Lipid Metabolism / Q000235:genetics* / Q000502:physiology; D008055:Lipids / Q000235:genetics*; D008099:Liver / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D017686:Oncorhynchus mykiss / Q000235:genetics* / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019893:Ribosomal Protein S6 Kinases / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D051780:Sterol Regulatory Element Binding Protein 1; D058570:TOR Serine-Threonine Kinases
D007328:Insulin; D008055:Lipids; D051780:Sterol Regulatory Element Binding Protein 1; D005954:Glucosephosphate Dehydrogenase; D064429:Fatty Acid Synthases; D011494:Protein Kinases; D051057:Proto-Oncogene Proteins c-akt; D019893:Ribosomal Protein S6 Kinases; D058570:TOR Serine-Threonine Kinases; D012695:L-Serine Dehydratase