LAUSR

When fasted as larvae or fed ketogenic diets as adults, homozygous zebrafish slc16a6a mutants develop hepatic steatosis because their livers cannot export the major ketone body β-hydroxybutyrate, diverting liver-trapped ketogenic carbon atoms to triacylglycerol. Here, we find that slc16a6a mutants are longer than their wild-type siblings. This effect is largely not sexually dimorphic, nor is it affected by dietary fat content on a pure genetic background. A mixed genetic background alters the proportionality of mass to length modestly. We also observe that non-coding variations in the 5′-untranslated region and first intron, and coding variations within the fifth exon of the orthologous human gene locus SLC16A6 are highly significantly associated with human height. Since both zebrafish and human orthologs of SLC16A6 are expressed in multiple locations, this gene likely regulates height through modulating transport of monocarboxylic acids in several tissues.