Fatty acid binding proteins--the evolutionary crossroads of inflammatory and metabolic responses - PubMed (original) (raw)

Review

Fatty acid binding proteins--the evolutionary crossroads of inflammatory and metabolic responses

Liza Makowski et al. J Nutr. 2004 Sep.

Abstract

Fatty acid binding proteins (FABPs) are members of a highly conserved family of proteins with the task of protecting a cell's delicate lipid balance. Yet they fail when faced with metabolic or inflammatory stress, turning the cytosol into an inhospitable environment with less than ideal outcomes. This review will focus on how FABPs direct lipid traffic and simultaneously control inflammatory and metabolic pathways under the pressures of the Metabolic Syndrome.

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Figures

FIGURE 1

FIGURE 1

A model demonstrating FABPs at the crossroads of inflammatory and metabolic signaling pathways. Fatty acids are liberated by lipase activity from lipoprotein particles (LPL), membranes (PLA2), and lipid droplets (HSL), or delivered into the cell through membrane transporters like CD36. FABP may regulate 1) the generation, distribution, and coupling of these lipid signals to their biological targets through direct interaction with enzymes such as HSL, 2) the delivery of ligands to the nucleus, and/or 3) the sequestration of lipid mediators such as fatty acids, eicosanoids, or oxysterols. Potential lipid-sensitive targets linked to inflammation and insulin signaling include stress-activated kinases such as JNK and IKK/NF_κ_B, and nuclear hormone receptors such as PPAR_γ_ and LXR_α_. Although the mechanisms are unclear, this model suggests that FABPs control the lipid balance in inflammatory and metabolic cells like macrophages and adipocytes to alter the formation of components of the Metabolic Syndrome.

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