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Intake of trans fatty acids causes nonalcoholic steatohepatitis and reduces adipose tissue fat content.

Abstract

We investigated the effects of dietary trans fatty acids, PUFA, and SFA on body and liver fat content, liver histology, and mRNA of enzymes involved in fatty acid metabolism. LDL receptor knockout weaning male mice were fed for 16 wk with diets containing 40% energy as either trans fatty acids (TRANS), PUFA, or SFA. Afterwards, subcutaneous and epididymal fat were weighed and histological markers of nonalcoholic fatty liver disease (NAFLD) were assessed according to the Histological Scoring System for NAFLD. PPARalpha, PPARgamma, microsomal triglyceride transfer protein (MTP), carnitine palmitoyl transferase 1 (CPT-1), and sterol regulatory element binding protein-1c (SREBP-1c) mRNA were measured by quantitative RT-PCR. Food intake was similar in the 3 groups, although mice fed the TRANS diet gained less weight than those receiving the PUFA diet. Compared with the PUFA- and SFA-fed mice, TRANS-fed mice had greater plasma total cholesterol (TC) and triglyceride (TG) concentrations, less epididymal and subcutaneous fat, larger livers with nonalcoholic steatohepatitis (NASH)-like lesions, and greater liver TC and TG concentrations. Macrosteatosis in TRANS-fed mice was associated with a higher homeostasis model assessment of insulin resistance (HOMA(IR)) index and upregulated mRNA related to hepatic fatty acid synthesis (SREBP-1c and PPARgamma) and to downregulated MTP mRNA. Diet consumption did not alter hepatic mRNA related to fatty acid oxidation (PPARalpha and CPT-1). In conclusion, compared with PUFA- and SFA-fed mice, TRANS-fed mice had less adiposity, impaired glucose tolerance characterized by greater HOMA(IR) index, and NASH-like lesions due to greater hepatic lipogenesis. These results demonstrate the role of trans fatty acid intake on the development of key features of metabolic syndrome.

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  • Authors+Show Affiliations

    ,

    Endocrinology and Metabolism Division, Faculty of Medical Sciences, University of Sao Paulo, Sao Paulo, Brazil.

    , , , , , , , , ,

    Source

    The Journal of nutrition 140:6 2010 Jun pg 1127-32

    MeSH

    Adipose Tissue
    Animals
    Blood Glucose
    Dietary Fats
    Fatty Acids
    Fatty Acids, Unsaturated
    Fatty Liver
    Insulin
    Lipoproteins
    Male
    Metabolic Syndrome
    Mice
    Mice, Knockout
    Receptors, LDL
    Trans Fatty Acids

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    20357081

    Citation

    Machado, Roberta M., et al. "Intake of Trans Fatty Acids Causes Nonalcoholic Steatohepatitis and Reduces Adipose Tissue Fat Content." The Journal of Nutrition, vol. 140, no. 6, 2010, pp. 1127-32.
    Machado RM, Stefano JT, Oliveira CP, et al. Intake of trans fatty acids causes nonalcoholic steatohepatitis and reduces adipose tissue fat content. J Nutr. 2010;140(6):1127-32.
    Machado, R. M., Stefano, J. T., Oliveira, C. P., Mello, E. S., Ferreira, F. D., Nunes, V. S., ... Lottenberg, A. M. (2010). Intake of trans fatty acids causes nonalcoholic steatohepatitis and reduces adipose tissue fat content. The Journal of Nutrition, 140(6), pp. 1127-32. doi:10.3945/jn.109.117937.
    Machado RM, et al. Intake of Trans Fatty Acids Causes Nonalcoholic Steatohepatitis and Reduces Adipose Tissue Fat Content. J Nutr. 2010;140(6):1127-32. PubMed PMID: 20357081.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Intake of trans fatty acids causes nonalcoholic steatohepatitis and reduces adipose tissue fat content. AU - Machado,Roberta M, AU - Stefano,José T, AU - Oliveira,Claudia P M S, AU - Mello,Evandro S, AU - Ferreira,Fabiana D, AU - Nunes,Valeria S, AU - de Lima,Vicência M R, AU - Quintão,Eder C R, AU - Catanozi,Sergio, AU - Nakandakare,Edna R, AU - Lottenberg,Ana Maria P, Y1 - 2010/03/31/ PY - 2010/4/2/entrez PY - 2010/4/2/pubmed PY - 2010/6/18/medline SP - 1127 EP - 32 JF - The Journal of nutrition JO - J. Nutr. VL - 140 IS - 6 N2 - We investigated the effects of dietary trans fatty acids, PUFA, and SFA on body and liver fat content, liver histology, and mRNA of enzymes involved in fatty acid metabolism. LDL receptor knockout weaning male mice were fed for 16 wk with diets containing 40% energy as either trans fatty acids (TRANS), PUFA, or SFA. Afterwards, subcutaneous and epididymal fat were weighed and histological markers of nonalcoholic fatty liver disease (NAFLD) were assessed according to the Histological Scoring System for NAFLD. PPARalpha, PPARgamma, microsomal triglyceride transfer protein (MTP), carnitine palmitoyl transferase 1 (CPT-1), and sterol regulatory element binding protein-1c (SREBP-1c) mRNA were measured by quantitative RT-PCR. Food intake was similar in the 3 groups, although mice fed the TRANS diet gained less weight than those receiving the PUFA diet. Compared with the PUFA- and SFA-fed mice, TRANS-fed mice had greater plasma total cholesterol (TC) and triglyceride (TG) concentrations, less epididymal and subcutaneous fat, larger livers with nonalcoholic steatohepatitis (NASH)-like lesions, and greater liver TC and TG concentrations. Macrosteatosis in TRANS-fed mice was associated with a higher homeostasis model assessment of insulin resistance (HOMA(IR)) index and upregulated mRNA related to hepatic fatty acid synthesis (SREBP-1c and PPARgamma) and to downregulated MTP mRNA. Diet consumption did not alter hepatic mRNA related to fatty acid oxidation (PPARalpha and CPT-1). In conclusion, compared with PUFA- and SFA-fed mice, TRANS-fed mice had less adiposity, impaired glucose tolerance characterized by greater HOMA(IR) index, and NASH-like lesions due to greater hepatic lipogenesis. These results demonstrate the role of trans fatty acid intake on the development of key features of metabolic syndrome. SN - 1541-6100 UR - https://www.unboundmedicine.com/medline/citation/20357081/Intake_of_trans_fatty_acids_causes_nonalcoholic_steatohepatitis_and_reduces_adipose_tissue_fat_content_ L2 - https://academic.oup.com/jn/article-lookup/doi/10.3945/jn.109.117937 DB - PRIME DP - Unbound Medicine ER -