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Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid.
J Nutr. 2004 Apr; 134(4):861-7.JN

Abstract

Decreased body fat mass and liver steatosis have been reported in mice fed diets containing the conjugated linoleic acid trans-10,cis-12-C18:2 (CLA2), but not in those fed diets containing cis-9,trans-11-C18:2 (CLA1). Because the decrease in fatty acid (FA) oxidation may cause fat accumulation, we questioned whether the effects of both CLAs on enzyme activities and mRNA expression were related to liver FA oxidation. To address this question, 7-wk-old male C57BL/6J mice were fed for 4 wk a diet supplemented with 1% CLA1, CLA2, or cis-9-C18:1 (control) esterified as triacylglycerols. In CLA2-fed mice, the proportions of CLA2 in the total FA of liver lipids were substantially lower than those of CLA1 in mice fed CLA1. The mitochondrial protein content per total liver was about 56% greater in CLA2-fed mice than in CLA1-fed mice and controls. Mitochondrial carnitine palmitoyltransferase I (CPT I) and carnitine-dependent palmitate oxidation activities were also significantly greater in CLA2-fed mice than in the two other groups. The amounts of malonyl-CoA per gram of liver and the sensitivity of CPT I to malonyl-CoA inhibition were greater in both groups of CLA-fed mice than in the controls. L-CPT I mRNA expression doubled in CLA2-fed mice and was 3 and 2 times greater for M-CPT I in the CLA1 and CLA2 groups, respectively, compared with controls. Peroxisomal FA oxidation-related activities and acyl-CoA oxidase mRNA expression were increased in CLA1-fed mice, and to a larger extent in CLA2-fed mice, relative to controls. These data indicate that FA oxidation capacities were increased in mice fed CLA2, but were likely depressed in vivo through malonyl-CoA inhibition.

Authors+Show Affiliations

UPRES Lipides et Nutrition EA2422, Faculté des Sciences Gabriel, Université de Bourgogne, 21000 Dijon, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15051838

Citation

Degrace, P, et al. "Hepatic Steatosis Is Not Due to Impaired Fatty Acid Oxidation Capacities in C57BL/6J Mice Fed the Conjugated Trans-10,cis-12-isomer of Linoleic Acid." The Journal of Nutrition, vol. 134, no. 4, 2004, pp. 861-7.
Degrace P, Demizieux L, Gresti J, et al. Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid. J Nutr. 2004;134(4):861-7.
Degrace, P., Demizieux, L., Gresti, J., Chardigny, J. M., Sébédio, J. L., & Clouet, P. (2004). Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid. The Journal of Nutrition, 134(4), 861-7.
Degrace P, et al. Hepatic Steatosis Is Not Due to Impaired Fatty Acid Oxidation Capacities in C57BL/6J Mice Fed the Conjugated Trans-10,cis-12-isomer of Linoleic Acid. J Nutr. 2004;134(4):861-7. PubMed PMID: 15051838.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hepatic steatosis is not due to impaired fatty acid oxidation capacities in C57BL/6J mice fed the conjugated trans-10,cis-12-isomer of linoleic acid. AU - Degrace,P, AU - Demizieux,L, AU - Gresti,J, AU - Chardigny,J-M, AU - Sébédio,J-L, AU - Clouet,P, PY - 2004/3/31/pubmed PY - 2004/5/7/medline PY - 2004/3/31/entrez SP - 861 EP - 7 JF - The Journal of nutrition JO - J Nutr VL - 134 IS - 4 N2 - Decreased body fat mass and liver steatosis have been reported in mice fed diets containing the conjugated linoleic acid trans-10,cis-12-C18:2 (CLA2), but not in those fed diets containing cis-9,trans-11-C18:2 (CLA1). Because the decrease in fatty acid (FA) oxidation may cause fat accumulation, we questioned whether the effects of both CLAs on enzyme activities and mRNA expression were related to liver FA oxidation. To address this question, 7-wk-old male C57BL/6J mice were fed for 4 wk a diet supplemented with 1% CLA1, CLA2, or cis-9-C18:1 (control) esterified as triacylglycerols. In CLA2-fed mice, the proportions of CLA2 in the total FA of liver lipids were substantially lower than those of CLA1 in mice fed CLA1. The mitochondrial protein content per total liver was about 56% greater in CLA2-fed mice than in CLA1-fed mice and controls. Mitochondrial carnitine palmitoyltransferase I (CPT I) and carnitine-dependent palmitate oxidation activities were also significantly greater in CLA2-fed mice than in the two other groups. The amounts of malonyl-CoA per gram of liver and the sensitivity of CPT I to malonyl-CoA inhibition were greater in both groups of CLA-fed mice than in the controls. L-CPT I mRNA expression doubled in CLA2-fed mice and was 3 and 2 times greater for M-CPT I in the CLA1 and CLA2 groups, respectively, compared with controls. Peroxisomal FA oxidation-related activities and acyl-CoA oxidase mRNA expression were increased in CLA1-fed mice, and to a larger extent in CLA2-fed mice, relative to controls. These data indicate that FA oxidation capacities were increased in mice fed CLA2, but were likely depressed in vivo through malonyl-CoA inhibition. SN - 0022-3166 UR - https://www.unboundmedicine.com/medline/citation/15051838/Hepatic_steatosis_is_not_due_to_impaired_fatty_acid_oxidation_capacities_in_C57BL/6J_mice_fed_the_conjugated_trans_10cis_12_isomer_of_linoleic_acid_ L2 - https://academic.oup.com/jn/article-lookup/doi/10.1093/jn/134.4.861 DB - PRIME DP - Unbound Medicine ER -