| First Author | Lee SM | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 23118 | PubMed ID | 26984260 |
| Mgi Jnum | J:251801 | Mgi Id | MGI:6101520 |
| Doi | 10.1038/srep23118 | Citation | Lee SM, et al. (2016) Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia. Sci Rep 6:23118 |
| abstractText | 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( horizontal line / horizontal line ) 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. |
