N-acyl taurine (NAT)

N-acyl taurines (NATs) are a family of endogenous bioactive lipids consisting of a long-chain fatty acid tail N-linked to the amino group of the amino acid taurine [1]. These molecules function as signaling ligands that modulate the activity of several membrane proteins, most notably the Transient Receptor Potential (TRP) ion channels, specifically TRPV1 and TRPV4 [2]. By activating these channels, NATs participate in calcium signaling and sensory transduction related to pain and inflammation [4]. Beyond sensory roles, certain NAT species have been identified as endogenous chemical uncouplers of mitochondrial respiration, a process regulated by the enzyme PM20D1, which catalyzes their synthesis and hydrolysis [3]. This uncoupling activity indicates a significant role for NATs in systemic energy expenditure and thermogenesis, making them relevant to metabolic health [6]. Additionally, NATs have been observed to stimulate insulin secretion from pancreatic beta cells, further highlighting their importance in glucose homeostasis [5]. While NATs are bioactive metabolites rather than direct protein targets themselves, the enzymes that regulate their levels (such as FAAH and PM20D1) and the receptors they activate are major areas of investigation for treating obesity, type 2 diabetes, and chronic pain [3][5].

Other names

N-acyltaurinesFatty acid tauridesTaurine-conjugated fatty acidsN-acyl-taurines

N-acyl taurines act as endogenous agonists for Transient Receptor Potential (TRP) ion channels, specifically TRPV1 and TRPV4, and function as chemical uncouplers of mitochondrial oxidative phosphorylation to increase energy expenditure.