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High‐Carbohydrate Liquid Diet Induced Greater Severity in Hepatic Steatosis and Inflammatory Responses than High‐Fat Liquid Diet in Mice
Author(s) -
LI Xinli,
Lian Fuzhi,
Liu Chun,
Hu Kangquan,
Wang XiangDong
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.379.1
Subject(s) - steatosis , lipogenesis , medicine , endocrinology , fatty liver , carbohydrate , fatty acid synthase , chemistry , biology , lipid metabolism , disease
High fat diet is one of the dietary factors responsible for the development of hepatic steatosis, as the earliest stage of non‐alcoholic fatty liver disease (NAFLD). In the present study, we compared the effects of the Lieber‐DeCarli liquid diet (LD) with either high fat (HFLD, 22% and 60% energy from carbohydrates and fat, respectively) or high carbohydrate (HCLD, 70% and 12% energy from carbohydrates and fat, respectively) on development of hepatic steatosis and inflammatory responses in mice. C57BJ/6L mice (total n = 24) were group‐paired fed with two diets for 16 weeks. While there was no difference on average food intake and final body weight between HFLD and HCLD, we detected more severe hepatic steatosis in HCLD group (pathological steatosis grading 1 vs. 3 for HFLD vs. HCLD, p <0.05). As compared to HFLD, 1) HCLD feeding decreased hepatic protein levels of SIRT1, LKB1 and FOXO1; 2) HCLD up‐regulated both mRNA and protein expressions of ACC and SCD1 that related to de no lipogenesis (DNL); 3) HCLD down‐regulated mRNA expressions of CPT‐1, PPAR‐a, PGC1‐a genes related to fatty acid oxidation; and 4) HCLD increased hepatic inflammatory foci positivity (92.3% positive in HCLD group vs. 50% positive in HFLD group, p<0.05) which accompanied with significant increases of mRNA expressions of IL‐1b, TNF‐a and MCP‐1. In conclusions, under the similar intake of energy, HCLD induced greater severity in hepatic steatosis and inflammatory response than HFLD, potentially through down‐regulating SIRT1 and fatty acid oxidation and promoting DNL. Supported by the USDA/ARS 1950‐51000‐074S.