Ugt8a, also known as uridine diphosphate galactosyltransferase 8A, is potentially involved in glycolipid biosynthesis in vivo, especially in male-specific glycolipid production in the kidney [1]. It may be relevant to sex dependency in kidney diseases and is also associated with sphingolipid metabolism and TGF-β signaling pathway [1,4]. It could play a role in CNS lipid metabolism, specifically in the synthesis of myelin-associated lipids, and might be related to processes like myelin regeneration [5,6].

In a study on aging mice, integrated analysis of the kidney transcriptome identified Ugt8a as a potential enzyme for male-specific glycolipid biosynthesis, and inhibiting UGT8 reduced the levels of relevant glycolipids and inflammatory cytokines in the kidney [1]. In a mouse model of Sandhoff disease, the expression of Ugt8a was explored at different ages, but no significant difference in its expression levels related to myelination was found compared to control mice [2]. In multiple sclerosis experimental models, Ugt8a was among the down-regulated mutual genes [3]. In a non-alcoholic fatty liver disease (NAFLD) mouse model, transcriptomic analysis showed that Ugt8a was an important regulator associated with TGF-β signaling pathway and sphingolipid metabolism, and EAHP treatment affected its expression [4].

In summary, Ugt8a is potentially involved in glycolipid biosynthesis, sphingolipid metabolism, and TGF-β signaling. Mouse models in studies related to aging, neurodegenerative diseases, multiple sclerosis, and NAFLD have provided insights into its role in these biological processes and disease conditions, suggesting its importance in understanding these areas at a molecular level.