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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., Nguyen, D., Anand, M., Kant, R., Koehncke, C., Lisewski, U., Roepke, T.K., 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 |
| ISSN: | 2045-2322 |
| Publisher: | Nature Publishing Group |
| Volume: | 6 |
| Page Range: | 23118 |
| Date: | 17 March 2016 |
| Official Publication: | https://doi.org/10.1038/srep23118 |
| PubMed: | View item in PubMed |
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