Session: FP05-Lipids: Regulation & Mechanism of Disease
Room 133 (Moscone Center)
Poster Board SAT-723
Experimental Design: Adult C57BL6 male mice were fed a normal chow diet or HFD with 60% of calories derived from fat and received twice daily IP injections of 0.75 mg/kg BW of nicotine or saline for 10 weeks.
Results: Light and electron microscopy revealed markedly higher lipid accumulation with lower content of endoplasmic reticulum and glycogen in hepatocytes from mice on HFD plus nicotine, compared to mice on HFD alone. Addition of nicotine to HFD further resulted in an increase in the incidence of hepatocellular apoptosis and was associated with activation of caspase 2 (an initiator caspase working upstream of kinase activation and mitochondria-dependent apoptotic pathway), p38 mitogen-activated protein kinase (MAPK), induction of inducible nitric oxide synthase (iNOS), and perturbation of the BAX/BCL-2 ratio.
Conclusions: Together, our data indicate the involvement of caspase 2, p38 MAPK, and iNOS that though activation of intrinsic pathway signaling promotes hepatocellular apoptosis and further worsen HFD-induced hepatic steatosis in obese mice. Targeting the caspase 2-mediated death pathway may have a protective role in development and progression of NAFLD.
Nothing to Disclose: RI, IS, MD, CSS, TCF, APS
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