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. 2013 May 2;134(2):291–303. doi: 10.1093/toxsci/kft104

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Published by Oxford University Press on behalf of the Society of Toxicology 2013. This work is written by (a) US Government employee(s) and is in the public domain in the US.

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Fig. 6. — Leptin controls BDCM-induced alterations in glycolysis, gluconeogenesis, and lipid metabolism, thus aiding in development of liver injury in NASH. (A) mRNA expressions of liver Glut-1, PFK, and PCK-1 in DIO + BDCM and Leptin KO +BDCM groups. (B) mRNA expressions of liver PGC-1α, SREBP-1c, and PPAR-γ in DIO + BDCM and Leptin KO + BDCM groups. (C) Picro sirius red staining showing micro- and macrovesicular fibrosis (arrow) in DIO + BDCM (panel i) and Leptin KO + BDCM (panel ii) groups. (D) Hematoxylin and eosin staining showing hepatocellular necrosis (arrow) in DIO + BDCM (panel i) and Leptin KO + BDCM (panel ii) groups. (E) Serum ALT and AST enzyme levels in DIO + BDCM and Leptin KO + BDCM groups (n = 4). *p < 0.05 is considered statistically significant.