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 β 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.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Lee SM,Nguyen D,Anand M,Kant R,Köhncke C,Lisewski U,Roepke TK,Hu Z,Abbott GWdoi
10.1038/srep23118subject
Has Abstractpub_date
2016-03-17 00:00:00pages
23118issn
2045-2322pii
srep23118journal_volume
6pub_type
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