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Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia

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Item Type:Article
Title:Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia
Creators Name:Lee, S.M. and Nguyen, D. and Anand, M. and Kant, R. and Koehncke, C. and Lisewski, U. and Roepke, T.K. and Hu, Z. and Abbott, G.W.
Abstract:Nonalcoholic fatty liver disease (NAFLD) is an increasing health problem worldwide, with genetic, epigenetic, and environmental components. Here, we describe the first example of NAFLD caused by genetic disruption of a mammalian potassium channel subunit. Mice with germline deletion of the KCNE2 potassium channel {beta} subunit exhibited NAFLD as early as postnatal day 7. Using mouse genetics, histology, liver damage assays and transcriptomics we discovered that iron deficiency arising from KCNE2-dependent achlorhydria is a major factor in early-onset NAFLD in Kcne2(-/-) mice, while two other KCNE2-dependent defects did not initiate NAFLD. The findings uncover a novel genetic basis for NAFLD and an unexpected potential factor in human KCNE2-associated cardiovascular pathologies, including atherosclerosis.
Keywords:C-Reactive Protein, Gene Regulatory Networks, Germ-Line Mutation, High-Fat Diet, Homocysteine, Iron-Deficiency Anemia, Liver, Non-Alcoholic Fatty Liver Disease, Sequence Deletion, Transcriptome, Triglycerides, Voltage-Gated Potassium Channels, Animals, Mice
Source:Scientific Reports
Publisher:Nature Publishing Group
Page Range:23118
Date:17 March 2016
Official Publication:https://doi.org/10.1038/srep23118
PubMed:View item in PubMed

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