Recent insights into the biological functions of liver fatty acid binding protein 1

Wang, Guqi; Bonkovsky, Herbert L.; Lemos, Andrew de; Burczynski, Frank J.

doi:10.1194/jlr.r056705

Cited by 194 publications

(183 citation statements)

References 130 publications

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“…Collectively these observations indicate that AGP may deregulate liver lipid metabolism, an unexpected and perhaps undesirable consequence of AGP use. We showed that under conditions of immunological stress following C. rodentium challenge, mice not treated with AGP had decreased expression of 3-hydroxymethyl-3-methylglutaryl-CoA lyase ( Hmgcl ) and fatty acid binding protein 1 ( Fabp1 ) both of which are involved in lipogenesis5253. However, CR+ mice administered either CTC and TYL did not exhibit decreased expression of these metabolic genes.…”

Section: Discussionmentioning

confidence: 96%

Antimicrobial growth promoters modulate host responses in mice with a defined intestinal microbiota

Brown

Zaytsoff

Uwiera

et al. 2016

Sci Rep

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Antibiotics can promote growth in livestock (antimicrobial growth promoters, AGPs), however lack of knowledge regarding mechanisms has hampered the development of effective non-antibiotic alternatives. Antibiotics affect eukaryotic cells at therapeutic concentrations, yet effects of AGPs on host physiology are relatively understudied, partially due to the complexity of host-microorganism interactions within the gastrointestinal tract. To determine the direct effects of AGPs on the host, we generated Altered Schaedler Flora (ASF) mice, and administered chlortetracycline (CTC) and tylosin phosphate (TYL) in feed. Mice were challenged with Citrobacter rodentium to determine how AGPs alter host responses to physiological stress. Although CTC and TYL had inconsistent effects on the ASF taxa, AGPs protected mice from weight loss following C. rodentium inoculation. Mice treated with either CTC or TYL had lower expression of βd1 and Il17a in the intestine and had a robust induction of Il17a and Il10. Furthermore, AGP administration resulted in a lower hepatic expression of acute phase proteins (Saa1, Hp, and Cp) in liver tissue, and ameliorated C. rodentium-induced reductions in the expression of genes involved in lipogenesis (Hmgcl and Fabp1). Collectively, this indicates that AGPs directly affect host physiology, and highlights important considerations in the development of non-antibiotic alternatives.

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Section: Discussionmentioning

confidence: 96%

Antimicrobial growth promoters modulate host responses in mice with a defined intestinal microbiota

Brown

Zaytsoff

Uwiera

et al. 2016

Sci Rep

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“…The relatively high levels of fabp1b.2 in brain may be attributable to ligand preferences because it is known that polyunsaturated FAs are highly abundant in the central nervous system ( 66,67 ). Whole-mount in situ hybridization demonstrated high transcript levels of fabp1b ( fabp1b.1 plus fabp1b.2 ) and fabp2 in the anterior intestine, but no mRNAs were detected in the posterior drugs and xenobiotics, controlling their uptake and intracellular transport (i.e., FABPs act as chaperones) (13)(14)(15)(16)(17)57 ). The cephalocaudal patterning of FABP transcript expression in the mammalian intestine was conserved through evolution.…”

Section: Discussionmentioning

confidence: 99%

Fatty acid binding proteins have the potential to channel dietary fatty acids into enterocyte nuclei

Esteves

Knoll‐Gellida

Canclini

et al. 2016

Journal of Lipid Research

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“…FABP1 facilitates the transportation, storage, and utilization of fatty acids and their acyl-CoA derivatives and may exert a protective effect against lipotoxicity by binding otherwise cytotoxic free fatty acids and facilitating their oxidation or incorporation into triglycerides [31]. FABP1 also affects the expression of PPARα and PPARγ by mediating the transport of PPAR ligands to the nucleus of hepatocytes, and intracellular FABP1 concentrations are correlated with PPARα and PPARγ activities [32].…”

Section: Hepatic Lipid Uptakementioning

confidence: 99%

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

Ipsen

Lykkesfeldt

Tveden‐Nyborg

2018

Cell. Mol. Life Sci.

1,002

757

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Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.

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Recent insights into the biological functions of liver fatty acid binding protein 1

Cited by 194 publications

References 130 publications

Antimicrobial growth promoters modulate host responses in mice with a defined intestinal microbiota

Antimicrobial growth promoters modulate host responses in mice with a defined intestinal microbiota

Fatty acid binding proteins have the potential to channel dietary fatty acids into enterocyte nuclei

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

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