Lipocalin-type prostaglandin D synthase was previously known as β-trace protein (BTP), a low-molecular-weight glycoprotein that is heavily expressed in human cerebrospinal fluid. Nevertheless, it is also seen to be expressed in numerous other tissues including the kidney, liver, lung, heart, adipose, muscle, and pancreas. Functionally, L-PGDS behaves like a lipocalin type protein where it helps in binding and transportation of small lipophilic substances, such as steroids, retinoids, and other lipophilic ligands. Enzymatically, L-PGDS functions as a prostaglandin synthase where it helps in the production of PGD2 by catalyzing the isomerization of PGH2, a common precursor of the two series of prostaglandins. PGD2 regulates its physiological function through two individual receptors named DP1 and DP2. L-PGDS has been a central player in many diseases, its role in metabolism including diabetes, fatty liver disease, and obesity has gathered a large attention. In this review, we summarize the current state of knowledge about L-PGDS and it's signaling in adipose, hepatic, skeletal muscle, and pancreas tissues, which are core targets for metabolic studies. Modulation of L-PGDS signaling can be considered as a potential future therapeutic target for the treatment of insulin resistance as well as fatty liver disease.
Keywords: Adipocytes; Insulin Resistance; L-PGDS; Non-Alcoholic Fatty Liver Disease (NAFLD); Obesity; Skeletal Muscle Atrophy.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.