Fat storage-inducing transmembrane protein 2 (FITM2)

Fat storage-inducing transmembrane protein 2 (FITM2) is an evolutionarily conserved enzyme and transmembrane protein residing in the endoplasmic reticulum, primarily found in adipose tissue[1][3][6][7]. FITM2 is essential for the partitioning of triglycerides into lipid droplets and thereby for neutral lipid storage and energy reserves. It acts as a fatty acyl–coenzyme A diphosphatase, and its enzymatic activity is critical for preserving ER structure and lipid droplet biogenesis. FITM2 is regulated by PPARγ, a key transcription factor for adipocyte differentiation, and is indispensable for normal fat storage and metabolic function. Loss or deficiency of FITM2 leads to progressive lipodystrophy, impaired lipid homeostasis, ER stress, metabolic dysfunction, and—in humans—neurological syndromes such as deafness–dystonia. No drugs directly targeting FITM2 are currently known, but its central role in lipid metabolism makes it a potential therapeutic target and biomarker in metabolic and adipocyte-related diseases[1][2][4][5].

Other names

FIT2Acyl-coenzyme A diphosphatase FITM2C20orf142dJ881L22.2Fat-inducing protein 2Fat-inducing transcript 2SIDDIS

Drugs targeting FITM2 would potentially modulate lipid droplet formation by regulating triglyceride partitioning or acyl-CoA hydrolysis Mechanisms are hypothetical, as no direct FITM2-targeted drugs are described