Skip to main content
. Author manuscript; available in PMC: 2024 Jul 23.
Published in final edited form as: FASEB J. 2023 Mar;37(3):e22825. doi: 10.1096/fj.202201972RR

FIGURE 3.

FIGURE 3

Role of eNAMPT in preclinical murine model of STZ/HFD-induced hepatic steatosis and NASH. (A) IHC for NAMPT showing low levels of NAMPT expression as mild staining in the control normal liver hepatocytes (Murine normal). NAMPT hepatic expression was markedly increased in NAFLD STZ/HFD livers showing strong NAMPT IHC staining in hepatocytes (Murine STZ/HFD). (B) Quantitation of NAMPT immunostaining intensity in hepatocytes showed significantly higher NAMPT expression levels in NAFLD STZ/HFD livers compared to normal control murine livers (n = 20, p < .05). (C) H&E staining showing normal liver in mice with control diet (Murine Normal). Control STZ/HFD mice developed pathological livers with severe pericentral/perivenous macrovesicular and microvesicular steatosis. STZ/HFD mice treated with IP anti-eNAMPT ALT-100 mAb, 0.4 mg/kg for 4 weeks, show marked reduction in hepatic steatosis. Control STZ/HFD mice were administered IP IgG with an identical dosing schedule. (D–G) Quantitative measures of the steatosis score (D), liver triglyceride level (E), liver-to-body weight ratio (F), and NAFLD activity score (NAS) (G) were significantly reduced in IP ALT-100 mAb-treated NAFLD mice compared to disease control NAFLD mice treated with IP IgG (p < .05, respectively) (bar—20 μm).