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Fatty acid binding protein: stimulation of microsomal phosphatidic acid formation

C A Jolly1, T Hubbell, W D Behnke

  • 1Department of Physiology and Pharmacology, Texas A & M University 77843-4466, USA.

Insights

Fatty acid binding proteins (FABPs), including liver (L-FABP) and intestinal (I-FABP), significantly enhance phosphatidic acid formation in liver microsomes. This occurs by boosting the conversion of fatty acyl-CoA and glycerol 3-phosphate to phosphatidate.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Lipid Metabolism

Background:

  • Fatty acid binding proteins (FABPs) are involved in lipid transport and metabolism.
  • Microsomal phosphatidic acid formation is a crucial step in phospholipid synthesis.
  • The specific roles of L-FABP and I-FABP in this process require further elucidation.

Purpose of the Study:

  • To investigate the effect of L-FABP and I-FABP on key steps of microsomal phosphatidic acid formation.
  • To determine whether FABPs influence fatty acyl-CoA synthase activity.
  • To characterize the mechanism by which FABPs enhance phosphatidic acid synthesis.

Main Methods:

  • Purification of rat liver microsomes using size-exclusion chromatography.
  • Utilized recombinant FABPs to prevent cross-contamination.
  • Enzyme assays measuring fatty acyl-CoA synthase and phosphatidic acid formation.
  • Fluorescence spectroscopy to study FABP-ligand interactions.

Main Results:

  • Neither L-FABP nor I-FABP stimulated liver microsomal fatty acyl-CoA synthase.
  • Both L-FABP and I-FABP significantly enhanced the conversion of fatty acyl-CoA and glycerol 3-phosphate to phosphatidic acid (18-fold and 7-fold, respectively).
  • Evidence suggests I-FABP interacts with fatty acyl-CoA, potentially mediating the observed stimulation.

Conclusions:

  • L-FABP and I-FABP directly stimulate liver microsomal phosphatidic acid formation.
  • The stimulation is primarily due to enhanced synthesis of phosphatidate from fatty acyl-CoA and glycerol 3-phosphate.
  • FABP interaction with fatty acyl-CoA is implicated in the mechanism of stimulation.

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