The Mammalian Fatty Acid-binding Protein Multigene Family: Molecular and Genetic Insights into Function

Hertzel, Ann V.; Bernlohr, David A.

doi:10.1016/s1043-2760(00)00257-5

Cited by 375 publications

(305 citation statements)

References 50 publications

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“…FABPs associate with various lipids and are typically involved in the trafficking of fatty acids (23,24). In fact, it has been proposed that FABPs can inhibit ␤-oxidation by sequestering fatty acids (23). Interestingly, lbp-8 expression was repressed after food removal, with kinetics similar to that observed for induction of the fat mobilization genes acs-2, gei-7, and cpt-3 (see Fig.…”

Section: Fasting Affects Expression Of Genes That Encode Fatty Acid-bmentioning

confidence: 54%

“…Two fasting response genes, lbp-1 and lbp-8, share significant homology with mammalian FABPs (Table 1). FABPs associate with various lipids and are typically involved in the trafficking of fatty acids (23,24). In fact, it has been proposed that FABPs can inhibit ␤-oxidation by sequestering fatty acids (23).…”

Section: Fasting Affects Expression Of Genes That Encode Fatty Acid-bmentioning

confidence: 99%

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A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49

Gilst

Hadjivassiliou²,

Yamamoto³

2005

Proc. Natl. Acad. Sci. U.S.A.

254

285

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Appropriate response to nutritional stress is critical for animal survival and metabolic health. To better understand regulatory networks that sense and respond to nutritional availability, we developed a quantitative RT-PCR strategy to monitor changes in metabolic gene expression resulting from short-term food deprivation (fasting) in Caenorhabditis elegans. Examining 97 fat and glucose metabolism genes in fed and fasted animals, we identified 18 genes significantly influenced by food withdrawal in all developmental stages. Fasting response genes fell into multiple kinetic classes, with some genes showing significant activation or repression just 1 h after food was removed. As expected, fasting stimulated the expression of genes involved in mobilizing fats for energy production, including mitochondrial ␤-oxidation genes. Surprisingly, however, we found that other mitochondrial ␤-oxidation genes were repressed by food deprivation. Fasting also affected genes involved in mono-and polyunsaturated fatty acid synthesis: four desaturases were induced, and one stearoylCoA desaturase (SCD) was strongly repressed. Accordingly, fasted animals displayed considerable changes in fatty acid composition. Finally, nuclear receptor nhr-49 played a key role in nutritional response, enabling induction of ␤-oxidation genes upon food deprivation and facilitating activation of SCD in fed animals. Our characterization of a fasting response system and our finding that nhr-49 regulates a sector within this system provide insight into the mechanisms by which animals respond to nutritional signals.fasting ͉ fat metabolism ͉ HNF4 ͉ stearoyl-CoA desaturase P recise control of energy storage and consumption is essential for surviving periods of food deprivation. Regulatory networks that govern fat and glucose metabolism are optimized to expend carbohydrates and accumulate fat when food intake is abundant, and switch to the consumption of stored fat when food is scarce (1, 2). In mammals, an overnight fast stimulates fat breakdown for the production of energy, enabling maintenance of glucose supply for CNS function and yielding acetyl-CoA for ketone body synthesis (3, 4). Orchestration of the fasting response is critical, and mutations that disrupt it can cause potentially lethal hypoglycemia and hypoketonemia (4, 5). Indeed, even subtle misregulation of these pathways can bring about diabetes and obesity (1, 6).A complex network of hormonal signals and regulatory mechanisms governs adaptation to food availability. In mammals, much of the fasting response is transcriptionally regulated (7-9). Increased fat consumption is facilitated by the induction of genes involved in fatty acid ␤-oxidation, whereas repression of glycolysis genes and activation of gluconeogenic genes maintains glucose supply. Additionally, activation of ketogenic genes enhances conversion of fatty acid ␤-oxidation products into ketone bodies (3). Despite these general observations, studies of the fasting response have been limited to a select group of genes in only a subse...

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Section: Fasting Affects Expression Of Genes That Encode Fatty Acid-bmentioning

confidence: 54%

Section: Fasting Affects Expression Of Genes That Encode Fatty Acid-bmentioning

confidence: 99%

A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49

Gilst

Hadjivassiliou²,

Yamamoto³

2005

Proc. Natl. Acad. Sci. U.S.A.

254

285

View full text Add to dashboard Cite

show abstract

“…Fatty acid-binding proteins are a family of small intracellular lipid chaperones that reversibly bind hydrophobic ligands, such as long chain fatty acids and eicosanoids, facilitating the intracellular diffusion of fatty acids between cellular compartments and enzymes (1,2). Adipocyte fatty acid-binding protein (A-FABP, 3 also known as aP2 and FABP4) is a member of the fatty acid-binding protein family that is abundantly expressed in adipose tissue (1,2).…”

mentioning

confidence: 99%

Adipocyte Fatty Acid-binding Protein Modulates Inflammatory Responses in Macrophages through a Positive Feedback Loop Involving c-Jun NH2-terminal Kinases and Activator Protein-1

Hui

Zhou

et al. 2010

Journal of Biological Chemistry

149

140

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“…The FABP family consists of nine highly homologous proteins expressed with distinct tissue specificity (1). FABPs bind long-chain fatty acids and are believed to function as transporters of fatty acids to intracellular targets.…”

mentioning

confidence: 99%

Deficiency of Fatty Acid-Binding Proteins in Mice Confers Protection from Development of Experimental Autoimmune Encephalomyelitis

Reynolds

Liu

Brittingham

et al. 2007

The Journal of Immunology

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Fatty acid-binding proteins (FABPs) act as intracellular receptors for a variety of hydrophobic compounds, enabling their diffusion within the cytoplasmic compartment. Recent studies have demonstrated the ability of FABPs to simultaneously regulate metabolic and inflammatory pathways. We investigated the role of adipocyte FABP and epithelial FABP in the development of experimental autoimmune encephalomyelitis to test the hypothesis that these FABPs impact adaptive immune responses and contribute to the pathogenesis of autoimmune disease. FABP-deficient mice exhibited a lower incidence of disease, reduced clinical symptoms of experimental autoimmune encephalomyelitis and dramatically lower levels of proinflammatory cytokine mRNA expression in CNS tissue as compared with wild-type mice. In vitro Ag recall responses of myelin oligodendrocyte glycoprotein 35–55-immunized FABP−/− mice showed reduced proliferation and impaired IFN-γ production. Dendritic cells deficient for FABPs were found to be poor producers of proinflammatory cytokines and Ag presentation by FABP−/− dendritic cells did not promote proinflammatory T cell responses. This study reveals that metabolic-inflammatory pathway cross-regulation by FABPs contributes to adaptive immune responses and subsequent autoimmune inflammation.

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The Mammalian Fatty Acid-binding Protein Multigene Family: Molecular and Genetic Insights into Function

Cited by 375 publications

References 50 publications

A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49

A Caenorhabditis elegans nutrient response system partially dependent on nuclear receptor NHR-49

Adipocyte Fatty Acid-binding Protein Modulates Inflammatory Responses in Macrophages through a Positive Feedback Loop Involving c-Jun NH2-terminal Kinases and Activator Protein-1

Deficiency of Fatty Acid-Binding Proteins in Mice Confers Protection from Development of Experimental Autoimmune Encephalomyelitis

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