biostudies-literatureLei XNIDA NIH HHSNIDDK NIH HHSNational Institute of Diabetes and Digestive and Kidney DiseasesNIMH NIH HHSNINDS NIH HHSNational Institutes of Health14734-14747https://www.ebi.ac.uk/biostudies/studies/S-EPMC6894063biostudies-literatureUnknown33(12)Cytokines and chemokines play diverse roles in different organ systems. Family with sequence similarity 19, member A1-5 (FAM19A1-A5; also known as TAFA1-5) is a group of conserved chemokine-like proteins enriched in the CNS of mice and humans. Their functions are only beginning to emerge. Here, we show that the expression of <i>Fam19a1-a5</i> in different mouse brain regions are induced or suppressed by unfed and refed states. The striking nutritional regulation of <i>Fam19a</i> family members in the brain suggests a potential central role in regulating metabolism. Using a knockout (KO) mouse model, we show that loss of FAM19A1 results in sexually dimorphic phenotypes. In male mice, FAM19A1 deficiency alters food intake patterns during the light and dark cycle. <i>Fam19a1</i> KO mice are hFASEB journal : official publication of the Federation of American Societies for Experimental BiologyFAM19A1, a brain-enriched and metabolically responsive neurokine, regulates food intake patterns and mouse behaviors.PMC6894063R01 DA041208T32 NS091018R01 DK084171DK084171R01 MH083728Liu LDong XLei XCisternas PWong GWLay MMartinelli DCKaruppagounder SSAja SPletnikov MVTerrillion CEfalseFAM19A1, a brain-enriched and metabolically responsive neurokine, regulates food intake patterns and mouse behaviors.Cytokines and chemokines play diverse roles in different organ systems. Family with sequence similarity 19, member A1-5 (FAM19A1-A5; also known as TAFA1-5) is a group of conserved chemokine-like proteins enriched in the CNS of mice and humans. Their functions are only beginning to emerge. Here, we show that the expression of <i>Fam19a1-a5</i> in different mouse brain regions are induced or suppressed by unfed and refed states. The striking nutritional regulation of <i>Fam19a</i> family members in the brain suggests a potential central role in regulating metabolism. Using a knockout (KO) mouse model, we show that loss of FAM19A1 results in sexually dimorphic phenotypes. In male mice, FAM19A1 deficiency alters food intake patterns during the light and dark cycle. <i>Fam19a1</i> KO mice are h2019-01-01T00:00:00Z2019 Dec2025-04-19T04:31:09.054Z2021-02-20T00:24:08ZS-EPMC68940633168937210.1096/fj.201901232RR10.1096/fj.201901232rr