Disease relevance of SLC27A4

• RESULTS: In acquired obesity FATP4 expression was up-regulated independently of genetic background (DeltaFATP4 versus DeltaBMI; r=0.50, p=0.04; DeltaFATP4 versus Deltabody fat; r=0.59, p=0.01) [1].

High impact information on SLC27A4

• New data reveal that insulin may regulate this process in part by promoting membrane trafficking of intracellular fatty acid transporters FATP1 and FATP4 to the plasma membrane [2].
• However, this is dependent on the enzymatic activity of FATP4, catalyzing the esterification of fatty acids with CoA [3].
• Here, we show that FATP4 is in fact localized to the endoplasmic reticulum and not the plasma membrane as reported previously [3].
• CONCLUSIONS/INTERPRETATION: These findings indicate that expression of specific adipose tissue fatty-acid-handling proteins is related to obesity and insulin resistance, and that, in particular, FATP4 plays a role in acquired obesity [1].
• However, the mRNA expression of FATP-1 and FATP-4 in placenta was correlated with DHA in both maternal plasma and placental phospholipids, although only FATP-4 expression was significantly correlated with DHA in cord blood phospholipids [4].

Biological context of SLC27A4

• We propose that the enzyme FATP4 drives fatty acid uptake indirectly by esterification [3].

Associations of SLC27A4 with chemical compounds

• A three-dimensional model of the FATP4 protein based on structural and functional similarity with adenylate-forming enzymes revealed that the variable residue 209 is exposed in a region potentially involved in protein-protein interactions [5].

References