Capillary Endothelial Fatty Acid Binding Proteins 4 and 5 Play a Critical Role in Fatty Acid Uptake in Heart and Skeletal Muscle

This article reviews our current understanding of the uptake of fatty acids by the enterocytes of the intestine. The micellar solubilization of fatty acids by bile salts and the factors regulating that process are discussed. The mechanism of how micellar solubilization of fatty acids promotes the uptake of fatty acids by enterocytes and their relative importance is reviewed. Additionally, discussion of the various fatty acid transporters located at the brush border membrane of the enterocytes is included. Finally, a summary of our current understanding of the function of fatty-acid-binding proteins inside enterocytes is provided.

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Discovery of genetic variants for fatty acid binding proteins of pig (Brief Report)

Archives Animal Breeding ◽

10.5194/aab-54-319-2011 ◽

2011 ◽

Vol 54 (3) ◽

pp. 319-322

Author(s):

H. Chung

Keyword(s):

Skeletal Muscle ◽

Signal Transduction ◽

Fatty Acid ◽

Genetic Variants ◽

Genetic Information ◽

Binding Proteins ◽

Fatty Acid Binding Proteins ◽

Signal Transduction Pathways ◽

Fatty Acid Binding ◽

Fat Thickness

Abstract. Back fat thickness (BFT) and intramuscular fat (IMF) contents are known as major issues affecting meat performance. Several types of fatty acid-binding proteins (FABPs), which involve signal transduction pathways, are abundantly presented in tissues such as intestine, liver, kidney, mammary gland, heart, and red skeletal muscle (Nechtelberger et al. 2001). FABPs have been reported to be differentially expressed genes during porcine adipogenesis (Samulin et al. 2008) and related to fat deposition (Szczerbal et al. 2007). Accordingly FABPs may be candidate genes to explain variation of fat related traits in pigs. Therefore, it is an essential process to search genetic variants that may provide useful genetic information to study associations with quantitative loci (QTL).

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Fatty Acid Binding Proteins in the Three Types of Rat Skeletal Muscle

Experimental Biology and Medicine ◽

10.3181/00379727-189-42795 ◽

1988 ◽

Vol 189 (2) ◽

pp. 183-188 ◽

Cited By ~ 18

Author(s):

W. C. Miller ◽

R. C. Hickson ◽

N. M. Bass

Keyword(s):

Skeletal Muscle ◽

Fatty Acid ◽

Binding Proteins ◽

Fatty Acid Binding Proteins ◽

Rat Skeletal Muscle ◽

Fatty Acid Binding

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Fatty-acid-binding proteins as a novel target for the treatment of anti-PD-1-resistant tumors.

Journal of Clinical Oncology ◽

10.1200/jco.2017.35.15_suppl.11562 ◽

2017 ◽

Vol 35 (15_suppl) ◽

pp. 11562-11562

Author(s):

James William Welsh ◽

Sharareh Niknam ◽

Jonathan E. Schoenhals ◽

Hampartsoum B. Barsoumian ◽

Ahmed I. A. Younes ◽

...

Keyword(s):

Fatty Acid ◽

Binding Proteins ◽

Enrichment Analysis ◽

Gene Set Enrichment Analysis ◽

Fatty Acid Binding Proteins ◽

Acid Oxidation ◽

Type I ◽

Acid Uptake ◽

Fatty Acid Binding

11562 Background: The mechanisms underlying immunosuppression and resistance to PD1 inhibitors in cancer are not well understood. We attempted to fill this gap with an integrated transcriptome analysis in an anti-PD1-resistant lung adenocarcinoma mouse model. The model was created by in vivo passage of 344SQ murine lung cancer cells (p53R172HΔg/+K-rasLA1/+) in a syngeneic host repeatedly dosed with anti-mouse PD1 antibodies. Anti-PD1-resistant 344SQ (344SQ_R) and 344SQ parental (344SQ_P) cells were then inoculated into syngeneic 129Sv/ev mice, which were then dosed twice with anti-PD1 or control IgG antibodies. Methods: Tumor tissues were collected and analyzed as follows: transcriptome with Affymetrix; protein levels by reverse phase protein array analysis; signature enrichment by gene set enrichment analysis; metabolome by mass spectrometry; and lipid content with fluorescent probes Oil O and BODIPY. We also isolated tumor-infiltrating immune cells for flow cytometry and gene expression analyses. Results: We identified lipid-related metabolic pathways as being the most highly enriched in anti-PD1-resistant tumors (344SQ_R) vs. their 344SQ_P counterparts; the resistant cells also had more lipid droplets than the 344SQ_P cells. The anti-PD1-resistant tumors overexpressed several genes involved in lipogenesis and fatty acid pathways, including fatty acid binding proteins (FABPs). Specifically, FABP overexpression promoted fatty acid uptake and lipid-droplet accumulation in resistant tumors. 344SQ_R tumors promoted immune suppressive cells by upregulating FABPs expression in M2-like macrophages, marked by increased fatty acid intake and fatty acid oxidation. Conversely, percentages of CD4+ and CD8+ tumor-infiltrating lymphocytes were reduced in the resistant tumors. Conclusions: These results suggest that lipid metabolic rewiring drives resistance PD1 inhibitors supporting the accumulation of immunosuppressive cells, including M2-like macrophages, preventing type I immune responses elicited by T cells. Collectively, these findings reveal new potential lipid-related targets for drug development or new treatments combining inhibitors of these targets with anti-PD1 therapy.

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