Links between enhanced fatty acid flux, protein kinase C and NFκB activation, and apoB–lipoprotein production in the fructose-fed hamster model of insulin resistance
作者： Rafik Ragheb , Amina M. Medhat , Gamila M.L. Shanab , Dina M. Seoudi , I.G. Fantus
DOI: 10.1016/J.BBRC.2008.03.044
关键词: Lipoprotein 、 Hamster 、 Ex vivo 、 Apolipoprotein B 、 Protein kinase C 、 Fructose 、 Fatty acid 、 Internal medicine 、 Biology 、 Insulin resistance 、 Endocrinology
摘要: Abstract In the current study, we show evidence, in a fructose-fed hamster model of insulin resistance, that free fatty acid (FFA) can induce hepatic resistance part via PKC activation leading to increased production atherogenic apoB100-containing lipoproteins. Interestingly, IκB-kinase β (IKKβ)-dependent NF-κB was activated hepatocytes from as an indication for activation. Treatment with oleate 16 h showed isoforms, PKCα/βII, dose dependent manner. Strikingly, general inhibitor, bisindolylmaleimide-I, Bis-I (5 μM) found ameliorate fructose-induced restoring phosphorylation status PKB and suppressing apoB100 overproduction ex vivo vivo. The data suggest activation, induced by circulating FFA may be important factor development dyslipidemia seen model.
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