Fig. 3: Overexpression and restoration of Acot12 alleviates NAFLD in HFHCD Acot12−/− mice.
From: Loss of Acot12 contributes to NAFLD independent of lipolysis of adipose tissue
a Eight-week-old normal C57BL/6 male mice fed an HFHCD for 14 weeks were injected with lentivirus containing control vector (lenti-con) or HA-tagged Acot12 vector (HA-Acot12) after 8 weeks of HFHCD feeding (n = 4). Representative liver image of immunostaining of HA-tag, H&E, Sirius Red, Oil Red O, and filipin staining in C57BL/6 mice injected with lentiviruses containing HA-Acot12 or control vector (lenti-con). A magnified image shows the HA-negative site and HA-positive site in HA-Acot12-injected mice. Scale bars, 200 μm. b Hepatic TG, TC, acetyl-CoA, and malonyl CoA levels of lenti-con- or HA-Acot12-injected 14-week HFHCD Acot12+/+ mice. c Expression level of genes related to lipogenesis (upper) and cholesterol metabolism (lower) in lenti-con- or HA-Acot12-injected 14-week HFHCD Acot12+/+ mouse livers (n = 4). d Eight-week-old male Acot12−/− mice injected with lentivirus containing lenti-con or HA-Acot12. After injection, both mouse groups were fed an HFHCD for 8 weeks (n = 4). Representative liver image of immunostaining of HA and H&E, Sirius Red, Oil red O, and filipin staining in HFHCD Acot12−/− mice injected with HA-Acot12 or lenti-con. Scale bars, 200 μm. e Hepatic TG, TC, acetyl-CoA, and malonyl-CoA levels of lenti-con- or HA-Acot12-injected Acot12−/− mice fed an HFHCD for 8 weeks. f Expression level of genes related to lipogenesis (upper) and cholesterol metabolism (lower) in lenti-con- or HA-Acot12-injected 8-week HFHCD Acot12−/− mouse livers (n = 4). All data are presented as the mean ± SEM. Statistical differences between two groups were determined using unpaired two-tailed Student’s t test (b, e) or multiple comparison tests followed by the Holm–Sidak method. c, f *P < 0.05; **P < 0.01; ****P < 0.0001.
