Fatty acid-binding protein and its relation to fatty acid oxidation

1993 ◽  
pp. 101-106 ◽  
Author(s):  
J. H. Veerkamp ◽  
H. T. B. van Moerkerk
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

scholarly journals The involvement of fatty acid binding protein in peroxisomal fatty acid oxidation

FEBS Letters ◽  
1990 ◽  
Vol 267 (2) ◽  
pp. 229-230 ◽  
Author(s):  
F.A.G. Reubsaet ◽  
J.H. Veerkamp ◽  
M.L.P. Brückwilder ◽  
J.M.F. Trijbels ◽  
L.A.H. Monnens
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Peroxisomal Fatty Acid Oxidation ◽  
Peroxisomal Fatty Acid

Fatty acid oxidation capacity and fatty acid-binding protein content of different cell types isolated from rat heart

1990 ◽  
Vol 98 (1-2) ◽  
pp. 19-25 ◽  
Author(s):  
M. C. J. G. Linssen ◽  
M. M. Vork ◽  
Y. F. de Jong ◽  
J. F. C. Glatz ◽  
G. J. van der Vusse
Keyword(s):  
Fatty Acid ◽  
Protein Content ◽  
Fatty Acid Oxidation ◽  
Rat Heart ◽  
Fatty Acid Binding Protein ◽  
Cell Types ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Different Cell Types

scholarly journals Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Yuting Chen ◽  
Yue Dai ◽  
Kaixin Song ◽  
Yi Huang ◽  
Le Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Binding Protein ◽  
Kidney Diseases ◽  
Binding Protein ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Kidney Fibrosis ◽  
Pharmacological Inhibition ◽  
Acid Binding Protein

AbstractKidney fibrosis is a hallmark of chronic kidney disease (CKD) progression that is caused by tubular injury and dysregulated lipid metabolism. Genetic abolition fatty acid-binding protein 4 (FABP4), a key lipid transporter, has been reported to suppress kidney interstitial fibrosis. However, the role and underlying mechanism of chemical inhibition of FABP4 in fibrotic kidney have not been well-documented. Here, we examined preemptive the effect of a FABP4 inhibitor, BMS309403, on lipid metabolism of tubular epithelial cells (TECs) and progression of kidney fibrosis. The expression of FABP4 was significantly elevated, concomitated with the accumulation of lipid droplets in TECs during kidney fibrosis. Treatment with BMS309403 alleviated lipid deposition of TECs, as well as interstitial fibrotic responses both in unilateral ureteral obstruction (UUO)-engaged mice and TGF-β-induced TECs. Moreover, BMS309403 administration enhanced fatty acid oxidation (FAO) in TECs by regulating peroxisome proliferator-activated receptor γ (PPARγ) and restoring FAO-related enzyme activities; In addition, BMS309403 markedly reduced cell lipotoxicity, such as endoplasmic reticulum (ER) stress and apoptosis in fibrotic kidney. Taken together, our results suggest that preemptive pharmacological inhibition of FABP4 by BMS309403 rebalances abnormal lipid metabolism in TECs and attenuates the progression of kidney fibrosis, thus may hold therapeutic potential for the treatment of fibrotic kidney diseases.

Sign in / Sign up

Export Citation Format

Share Document