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N-3 polyunsaturated fatty acids ameliorate hepatic steatosis via the PPAR-α/CPT-1α pathway in a mouse model of parenteral nutrition.
Biochem Biophys Res Commun 2018; 501(4):974-981BB

Abstract

Parenteral nutrition (PN) is one of the basic therapies for patients with intestinal failure; however, hepatic steatosis associated with PN limits the long-term use of PN. N-3 polyunsaturated fatty acids (PUFAs) have been used to improve clinical outcomes of patients receiving PN; however, the mechanisms by which n-3 PUFAs ameliorate hepatic steatosis remain unclear. In the present study, C57BL/6J mice were randomly assigned to three treatment groups, namely, enteral nutrition (EN), n-3 PUFAs, and n-6 PUFAs. Additionally, MK 886 was used to inhibit PPAR-α. After 7 days of intervention, mice were sacrificed, and liver tissue and serum samples were collected. Results from liver weight and liver triglyceride measurements and Oil Red O staining showed that n-3 PUFAs significantly reduced the liver triglyceride levels. In addition, treatment with n-3 PUFAs resulted in a greater decrease in serum triglyceride and low-density lipoprotein cholesterol levels compared to n-6 PUFAs. The key enzymes involved in FA oxidation, namely, PPAR-α and CPT-1α, were significantly restored at both the mRNA and protein levels in the n-3 PUFAs group. However, the benefits of n-3 PUFAs in improving serum and liver TG levels were abolished when the PPAR-α/CPT-1α pathway was blocked by MK 886. The results of this study indicated that n-3 PUFAs ameliorated the PN-associated hepatic steatosis by activating the PPAR-α/CPT-1α pathway. The present study provided a reliable scientific basis supporting the potential beneficial effects of n-3 PUFAs for improving hepatic steatosis in patients receiving long-term parenteral nutrition.

Authors+Show Affiliations

Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Southern Medical University, 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China. Electronic address: zlshe1107@163.com.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China. Electronic address: wxinying@263.net.

Pub Type(s)

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

Language

eng

PubMed ID

29777706

Citation

Tian, Feng, et al. "N-3 Polyunsaturated Fatty Acids Ameliorate Hepatic Steatosis Via the PPAR-α/CPT-1α Pathway in a Mouse Model of Parenteral Nutrition." Biochemical and Biophysical Research Communications, vol. 501, no. 4, 2018, pp. 974-981.
Tian F, Wang J, Sun H, et al. N-3 polyunsaturated fatty acids ameliorate hepatic steatosis via the PPAR-α/CPT-1α pathway in a mouse model of parenteral nutrition. Biochem Biophys Res Commun. 2018;501(4):974-981.
Tian, F., Wang, J., Sun, H., Yang, J., Wang, P., Wan, S., ... Wang, X. (2018). N-3 polyunsaturated fatty acids ameliorate hepatic steatosis via the PPAR-α/CPT-1α pathway in a mouse model of parenteral nutrition. Biochemical and Biophysical Research Communications, 501(4), pp. 974-981. doi:10.1016/j.bbrc.2018.05.095.
Tian F, et al. N-3 Polyunsaturated Fatty Acids Ameliorate Hepatic Steatosis Via the PPAR-α/CPT-1α Pathway in a Mouse Model of Parenteral Nutrition. Biochem Biophys Res Commun. 2018 07 2;501(4):974-981. PubMed PMID: 29777706.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-3 polyunsaturated fatty acids ameliorate hepatic steatosis via the PPAR-α/CPT-1α pathway in a mouse model of parenteral nutrition. AU - Tian,Feng, AU - Wang,Jiwei, AU - Sun,Haifeng, AU - Yang,Jianbo, AU - Wang,Peng, AU - Wan,Songlin, AU - Gao,Xuejin, AU - Zhang,Li, AU - Li,Jieshou, AU - Wang,Xinying, Y1 - 2018/05/21/ PY - 2018/05/13/received PY - 2018/05/14/accepted PY - 2018/5/20/pubmed PY - 2018/10/10/medline PY - 2018/5/20/entrez KW - Fatty liver KW - Lipid metabolism KW - Parenteral nutrition KW - n-3 PUFAs SP - 974 EP - 981 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 501 IS - 4 N2 - Parenteral nutrition (PN) is one of the basic therapies for patients with intestinal failure; however, hepatic steatosis associated with PN limits the long-term use of PN. N-3 polyunsaturated fatty acids (PUFAs) have been used to improve clinical outcomes of patients receiving PN; however, the mechanisms by which n-3 PUFAs ameliorate hepatic steatosis remain unclear. In the present study, C57BL/6J mice were randomly assigned to three treatment groups, namely, enteral nutrition (EN), n-3 PUFAs, and n-6 PUFAs. Additionally, MK 886 was used to inhibit PPAR-α. After 7 days of intervention, mice were sacrificed, and liver tissue and serum samples were collected. Results from liver weight and liver triglyceride measurements and Oil Red O staining showed that n-3 PUFAs significantly reduced the liver triglyceride levels. In addition, treatment with n-3 PUFAs resulted in a greater decrease in serum triglyceride and low-density lipoprotein cholesterol levels compared to n-6 PUFAs. The key enzymes involved in FA oxidation, namely, PPAR-α and CPT-1α, were significantly restored at both the mRNA and protein levels in the n-3 PUFAs group. However, the benefits of n-3 PUFAs in improving serum and liver TG levels were abolished when the PPAR-α/CPT-1α pathway was blocked by MK 886. The results of this study indicated that n-3 PUFAs ameliorated the PN-associated hepatic steatosis by activating the PPAR-α/CPT-1α pathway. The present study provided a reliable scientific basis supporting the potential beneficial effects of n-3 PUFAs for improving hepatic steatosis in patients receiving long-term parenteral nutrition. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/29777706/N_3_polyunsaturated_fatty_acids_ameliorate_hepatic_steatosis_via_the_PPAR_α/CPT_1α_pathway_in_a_mouse_model_of_parenteral_nutrition_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(18)31158-6 DB - PRIME DP - Unbound Medicine ER -