title: Effect of endurance training upon lipid metabolism in the liver of cachectic tumour-bearing rats.
abstract: The syndrome of cancer cachexia is accompanied by several alterations in lipid metabolism, and the liver is markedly affected. Previous studies showed that moderate exercise training may prevent liver fat accumulation through diminished delivery of lipids to the liver, increased hepatic oxidation and increased incorporation of triacylglycerol (TAG) into very low density lipoprotein (VLDL). Our aim was to examine the influence of moderate intensity training (8 weeks) upon TAG content, VLDL assembly and secretion, apolipoprotein B (apoB) and microsomal transfer protein (MTP) gene expression in the liver of cachectic tumour-bearing rats. Animals were randomly assigned to a sedentary control (SC), sedentary tumour-bearing (ST) or exercise-trained control (EC) or to an exercise trained tumour-bearing (ET) group. Trained rats ran on a treadmill (60% VO(2max)) for 60 min day(-1), 5 day week(-1), for 8 weeks. TAG content and the rate of VLDL secretion (followed for 3 h), as well as mRNA expression of apoB and MTP, and total cholesterol, VLDL-TAG, VLDL-cholesterol, high density lipoprotein cholesterol (HDL-cholesterol) and tumour weight were evaluated. VLDL-cholesterol showed a decrease in ST (p < 0.05) in relation to SC. Serum TAG, VLDL-TAG and tissue TAG content were all increased in ST (p < 0.01), when compared with SC. ST showed a lower rate of VLDL secretion (p < 0.05) and reduced expression of apoB (p < 0.001) and MTP (p < 0.001), when compared with SC. These parameters were restored to control values (p < 0.05) when the animals were submitted to the exercise training protocol. Tumour weight decreased 10-fold after training (p < 0.001). It is possible to affirm, therefore, that endurance training promoted the re-establishment of lipid metabolism in cachectic tumour-bearing animals, especially in relation to VLDL secretion and assembly.
authors.affiliation: Molecular Biology of the Cell Group, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
authors.forename: F S
authors.initials: FS
authors.lastname: Lira
authors.forename: F L
authors.initials: FL
authors.lastname: Tavares
authors.forename: A S
authors.initials: AS
authors.lastname: Yamashita
authors.forename: C H
authors.initials: CH
authors.lastname: Koyama
authors.forename: M J
authors.initials: MJ
authors.lastname: Alves
authors.forename: E C
authors.initials: EC
authors.lastname: Caperuto
authors.forename: M L
authors.initials: ML
authors.lastname: Batista
authors.forename: M
authors.initials: M
authors.lastname: Seelaender
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000235:genetics; D001835:Body Weight; D002100:Cachexia / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D002279:Carcinoma 256, Walker / Q000150:complications* / Q000473:pathology; D002352:Carrier Proteins / Q000235:genetics; D045744:Cell Line, Tumor; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D015870:Gene Expression; D050356:Lipid Metabolism / Q000502:physiology*; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011506:Proteins / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D001055:Apolipoproteins B; D002352:Carrier Proteins; D008076:Cholesterol, HDL; D015243:Cholesterol, VLDL; D008079:Lipoproteins, VLDL; D011506:Proteins; D014280:Triglycerides; C106092:microsomal triglyceride transfer protein; C030106:very low density lipoprotein triglyceride; D002784:Cholesterol