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Journal articles on the topic 'Human Liver Fatty Acid Binding Protein'

Author: Grafiati

Published: 11 March 2023

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1

Sharma, Ashwani, and Amit Sharma. "Fatty Acid Induced Remodeling within the Human Liver Fatty Acid-binding Protein." Journal of Biological Chemistry 286, no. 36 (July 8, 2011): 31924–28. http://dx.doi.org/10.1074/jbc.m111.270165.

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2

Cai, Jun, Christian Lücker, Zhongjing Chen, Elena Klimtchuk, Ye Qiao, and James A. Hamilton. "Human Liver Fatty Acid Binding Protein: Solution Structure and Ligand Binding." Biophysical Journal 96, no. 3 (February 2009): 600a. http://dx.doi.org/10.1016/j.bpj.2008.12.3140.

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3

Sheng, Nan, Juan Li, Hui Liu, Aiqian Zhang, and Jiayin Dai. "Interaction of perfluoroalkyl acids with human liver fatty acid-binding protein." Archives of Toxicology 90, no. 1 (November 5, 2014): 217–27. http://dx.doi.org/10.1007/s00204-014-1391-7.

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4

Cai, Jun, Christian Lücke, Zhongjing Chen, Ye Qiao, Elena Klimtchuk, and James A. Hamilton. "Solution Structure and Backbone Dynamics of Human Liver Fatty Acid Binding Protein: Fatty Acid Binding Revisited." Biophysical Journal 102, no. 11 (June 2012): 2585–94. http://dx.doi.org/10.1016/j.bpj.2012.04.039.

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5

Thumser, A. E., J. E. Voysey, and D. C. Wilton. "The binding of lysophospholipids to rat liver fatty acid-binding protein and albumin." Biochemical Journal 301, no. 3 (August 1, 1994): 801–6. http://dx.doi.org/10.1042/bj3010801.

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The binding of lysophospholipids to rat liver fatty acid-binding protein (FABP) and to BSA and human serum albumin was investigated by using competitive displacement fluorescence assays by monitoring the displacement of the fluorescent fatty acid probe 11-(dansylamino)undecanoic acid (DAUDA). In addition, direct binding assays using changes in tryptophan fluorescence were possible with albumin. Liver FABP was able to bind a range of lysophospholipids, oleoyl-lysophosphatidic acid (lysoPA), oleoyl-lysophosphatidylcholine (lysoPC), oleoyl-lysophosphatidylethanolamine (lysoPE) and oleoyl-lysophosphatidylglycerol, with similar affinity and a Kd of about 1 microM. Liver FABP was also able to bind lysophospholipids generated by the action of phospholipase A2 or phospholipase A1 (triacylglycerol lipase) on phospholipid vesicles. A possible physiological role for liver FABP in lysophospholipid metabolism within the cell is discussed. Albumin was shown to bind lysoPA with higher affinity than either lysoPC or lysoPE, and the initial minimal DAUDA displacement by lysoPA indicated that lysoPA was binding to the primary high-affinity fatty acid-binding sites on albumin and that, like oleic acid, about 3 mol of ligand/mol was bound to these sites. Kd values in the microM range were indicated for lysoPC and lysoPE, whereas, by comparison with oleic acid, the Kd for lysoPA was significantly lower and high-affinity binding in the nM range was indicated. Overall, the data suggest that, because of structural similarity, lysoPA binds to albumin in a similar manner to long-chain fatty acids.

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6

Favretto, Filippo, Carlo Santambrogio, Mariapina D'Onofrio, Henriette Molinari, Rita Grandori, and Michael Assfalg. "Bile salt recognition by human liver fatty acid binding protein." FEBS Journal 282, no. 7 (February 18, 2015): 1271–88. http://dx.doi.org/10.1111/febs.13218.

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7

Pietro, Santiago M. Di, and José A. Santomé. "Presence of two new fatty acid binding proteins in catfish liver." Biochemistry and Cell Biology 74, no. 5 (September 1, 1996): 675–80. http://dx.doi.org/10.1139/o96-073.

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A basic fatty acid binding protein (FABP), closely related to that of chicken liver, was isolated and characterized from catfish (Rhamdia sapo) liver in a previous work. Results herein show the presence of another two FABPs in which partial amino acid sequences reveal great similarity with the corresponding sequences of other already known FABPs belonging to the heart type. The purification procedures for both proteins involve gel filtration, anion-exchange chromatography, and sodium dodecyl sulfate – polyacrylamide gel electrophoresis (as a last step). Because both FABP N-termini were blocked, they were submitted to in-gel tryptic digestion and the resulting peptides were separated by high performance liquid chromatography, and sequenced by Edman degradation. One of these proteins presented the highest identity percentage when compared with those of the human and bovine heart and bovine brain (81%), and the other when compared with those of chicken retina (75%) and mouse and bovine heart FABP (70%). The presence of several FABPs plus the fact that they belong to different types, as found in the Rhamdia sapo liver, is unusual in mammals, which express a characteristic liver-type member of this protein family.Key words: fatty acid binding protein, liver, catfish, Rhamdia sapo.

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8

González, Javier M., and S. Zoë Fisher. "Structural analysis of ibuprofen binding to human adipocyte fatty-acid binding protein (FABP4)." Acta Crystallographica Section F Structural Biology Communications 71, no. 2 (January 28, 2015): 163–70. http://dx.doi.org/10.1107/s2053230x14027897.

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Inhibition of human adipocyte fatty-acid binding protein (FABP4) has been proposed as a treatment for type 2 diabetes, fatty liver disease and atherosclerosis. However, FABP4 displays a naturally low selectivity towards hydrophobic ligands, leading to the possibility of side effects arising from cross-inhibition of other FABP isoforms. In a search for structural determinants of ligand-binding selectivity, the binding of FABP4 towards a group of small molecules structurally related to the nonsteroidal anti-inflammatory drug ibuprofen was analyzed through X-ray crystallography. Several specific hydrophobic interactions are shown to enhance the binding affinities of these compounds, whereas an aromatic edge-to-face interaction is proposed to determine the conformation of bound ligands, highlighting the importance of aromatic interactions in hydrophobic environments.

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9

Velkov, Tony. "Interactions between Human Liver Fatty Acid Binding Protein and Peroxisome Proliferator Activated Receptor Selective Drugs." PPAR Research 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/938401.

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Fatty acid binding proteins (FABPs) act as intracellular shuttles for fatty acids as well as lipophilic xenobiotics to the nucleus, where these ligands are released to a group of nuclear receptors called the peroxisome proliferator activated receptors (PPARs). PPAR mediated gene activation is ultimately involved in maintenance of cellular homeostasis through the transcriptional regulation of metabolic enzymes and transporters that target the activating ligand. Here we show that liver- (L-) FABP displays a high binding affinity for PPAR subtype selective drugs. NMR chemical shift perturbation mapping and proteolytic protection experiments show that the binding of the PPAR subtype selective drugs produces conformational changes that stabilize the portal region of L-FABP. NMR chemical shift perturbation studies also revealed that L-FABP can form a complex with the PPAR ligand binding domain (LBD) of PPARα. This protein-protein interaction may represent a mechanism for facilitating the activation of PPAR transcriptional activity via the direct channeling of ligands between the binding pocket of L-FABP and the PPARαLBD. The role of L-FABP in the delivery of ligands directly to PPARαvia this channeling mechanism has important implications for regulatory pathways that mediate xenobiotic responses and host protection in tissues such as the small intestine and the liver where L-FABP is highly expressed.

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10

Cai, Jun, Christian Lücke, Ye Qiao, Elena Klimtchuk, and James A. Hamilton. "Solution Structure and Backbone Dynamics of Human Liver Fatty Acid Binding Protein." Biophysical Journal 98, no. 3 (January 2010): 238a. http://dx.doi.org/10.1016/j.bpj.2009.12.1288.

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11

Chen, S. H., P. Tuinen, D. H. Ledbetter, L. C. Smith, and L. Chan. "Human liver fatty acid binding protein gene is located on chromosome 2." Somatic Cell and Molecular Genetics 12, no. 3 (May 1986): 303–6. http://dx.doi.org/10.1007/bf01570790.

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12

Suzuki, Toshimitsu, Kazuo Watanabe, and Teruo Ono. "Immunohistochemical demonstration of liver fatty acid-binding protein in human hepatocellular malignancies." Journal of Pathology 161, no. 1 (May 1990): 79–83. http://dx.doi.org/10.1002/path.1711610113.

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13

Maatman, Ronald G. H. J., Herman T. B. van Moerkerk, Irene M. A. Nooren, Everardus J. J. van Zoelen, and Jacques H. Veerkamp. "Expression of human liver fatty acid-binding protein in Escherichia coli and comparative analysis of its binding characteristics with muscle fatty acid-binding protein." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1214, no. 1 (August 1994): 1–10. http://dx.doi.org/10.1016/0005-2760(94)90002-7.

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14

Martin, Gregory G., Danilo Landrock, Lawrence J. Dangott, Avery L. McIntosh, Ann B. Kier, and Friedhelm Schroeder. "Human Liver Fatty Acid Binding Protein-1 T94A Variant, Nonalcohol Fatty Liver Disease, and Hepatic Endocannabinoid System." Lipids 53, no. 1 (January 2018): 27–40. http://dx.doi.org/10.1002/lipd.12008.

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15

Maatman, R. G. H. J., T. H. M. S. M. Van Kuppevelt, and J. H. Veerkamp. "Two types of fatty acid-binding protein in human kidney. Isolation, characterization and localization." Biochemical Journal 273, no. 3 (February 1, 1991): 759–66. http://dx.doi.org/10.1042/bj2730759.

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Two types of fatty acid-binding protein (FABP) were isolated from human kidney by gel filtration and ion-exchange chromatography. Northern-blot analysis showed the presence of two FABP transcripts in total kidney RNA, hybridizing with cDNA of human liver and muscle FABP respectively. Characterisation based on molecular mass, isoelectric point, fluorescence with dansylaminoundecanoic acid and immunological cross-reactivity showed that one, type B, was fairly similar to human heart FABP. The other, type A, showed, like human liver FABP, a high fluorescence enhancement and a wavelength shift with dansylaminoundecanoic acid as well as the binding of a variety of ligands. Antibodies raised against FABP type A and against liver FABP markedly cross-reacted in e.l.i.s.a., in Western blotting and in indirect immunoperoxidase staining on kidney and liver sections. Differences in amino acid composition and isoelectric points, however, indicate that type A is a new kidney-specific FABP type. The FABP type A is more abundant in kidney than the B type and is predominantly localized in the cortex, especially in the cells of the proximal tubules. The FABP type B is mainly present in the cells of the distal tubules. In conclusion, this study shows the presence of two types of FABP in the kidney. One type seems to be related to heart FABP, while the other type resembles, but is not identical with, liver FABP. Both types have a characteristic cellular distribution along the nephron.

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16

Yang, Diwen, Jiajun Han, David Ross Hall, Jianxian Sun, Jesse Fu, Steven Kutarna, Keith A. Houck, et al. "Nontarget Screening of Per- and Polyfluoroalkyl Substances Binding to Human Liver Fatty Acid Binding Protein." Environmental Science & Technology 54, no. 9 (April 6, 2020): 5676–86. http://dx.doi.org/10.1021/acs.est.0c00049.

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17

Santambrogio, C., F. Favretto, M. D'Onofrio, M. Assfalg, R. Grandori, and H. Molinari. "Mass spectrometry and NMR analysis of ligand binding by human liver fatty acid binding protein." Journal of Mass Spectrometry 48, no. 8 (July 29, 2013): i. http://dx.doi.org/10.1002/jms.3191.

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18

Santambrogio, C., F. Favretto, M. D'Onofrio, M. Assfalg, R. Grandori, and H. Molinari. "Mass spectrometry and NMR analysis of ligand binding by human liver fatty acid binding protein." Journal of Mass Spectrometry 48, no. 8 (July 18, 2013): 895–903. http://dx.doi.org/10.1002/jms.3237.

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19

Long, Dong, and Daiwen Yang. "Buffer Interference with Protein Dynamics: A Case Study on Human Liver Fatty Acid Binding Protein." Biophysical Journal 96, no. 4 (February 2009): 1482–88. http://dx.doi.org/10.1016/j.bpj.2008.10.049.

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20

Chan, L., C. F. Wei, W. H. Li, C. Y. Yang, P. Ratner, H. Pownall, A. M. Gotto, and L. C. Smith. "Human liver fatty acid binding protein cDNA and amino acid sequence. Functional and evolutionary implications." Journal of Biological Chemistry 260, no. 5 (March 1985): 2629–32. http://dx.doi.org/10.1016/s0021-9258(18)89406-6.

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21

Liang, Kai, Ningning Li, Xiao Wang, Jianye Dai, Pulan Liu, Chu Wang, Xiao-Wei Chen, Ning Gao, and Junyu Xiao. "Cryo-EM structure of human mitochondrial trifunctional protein." Proceedings of the National Academy of Sciences 115, no. 27 (June 18, 2018): 7039–44. http://dx.doi.org/10.1073/pnas.1801252115.

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The mitochondrial trifunctional protein (TFP) catalyzes three reactions in the fatty acid β-oxidation process. Mutations in the two TFP subunits cause mitochondrial trifunctional protein deficiency and acute fatty liver of pregnancy that can lead to death. Here we report a 4.2-Å cryo-electron microscopy α2β2 tetrameric structure of the human TFP. The tetramer has a V-shaped architecture that displays a distinct assembly compared with the bacterial TFPs. A concave surface of the TFP tetramer interacts with the detergent molecules in the structure, suggesting that this region is involved in associating with the membrane. Deletion of a helical hairpin in TFPβ decreases its binding to the liposomes in vitro and reduces its membrane targeting in cells. Our results provide the structural basis for TFP function and have important implications for fatty acid oxidation related diseases.

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22

Huang, Huan, Avery L. McIntosh, Gregory G. Martin, Kerstin K. Landrock, Danilo Landrock, Shipra Gupta, Barbara P. Atshaves, Ann B. Kier, and Friedhelm Schroeder. "Structural and functional interaction of fatty acids with human liver fatty acid-binding protein (L-FABP) T94A variant." FEBS Journal 281, no. 9 (April 7, 2014): 2266–83. http://dx.doi.org/10.1111/febs.12780.

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23

McIntosh, Avery L., Huan Huang, Stephen M. Storey, Kerstin K. Landrock, Danilo Landrock, Anca D. Petrescu, Shipra Gupta, Barbara P. Atshaves, Ann B. Kier, and Friedhelm Schroeder. "Human FABP1 T94A variant impacts fatty acid metabolism and PPAR-α activation in cultured human female hepatocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 2 (July 15, 2014): G164—G176. http://dx.doi.org/10.1152/ajpgi.00369.2013.

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Although human liver fatty acid-binding protein (FABP1) T94A variant has been associated with nonalcoholic fatty liver disease and reduced ability of fenofibrate to lower serum triglycerides (TG) to target levels, molecular events leading to this phenotype are poorly understood. Cultured primary hepatocytes from female human subjects expressing the FABP1 T94A variant exhibited increased neutral lipid (TG, cholesteryl ester) accumulation associated with 1) upregulation of total FABP1, a key protein stimulating mitochondrial glycerol-3-phosphate acyltransferase (GPAM), the rate-limiting enzyme in lipogenesis; 2) increased mRNA expression of key enzymes in lipogenesis ( GPAM, LPIN2) in heterozygotes; 3) decreased mRNA expression of microsomal triglyceride transfer protein; 4) increased secretion of ApoB100 but not TG; 5) decreased long-chain fatty acid (LCFA) β-oxidation. TG accumulation was not due to any increase in LCFA uptake, de novo lipogenesis, or the alternate monoacylglycerol O-acyltransferase pathway in lipogenesis. Despite increased expression of total FABP1 mRNA and protein, fenofibrate-mediated FABP1 redistribution to nuclei and ligand-induced peroxisome proliferator-activated receptor (PPAR-α) transcription of LCFA β-oxidative enzymes (carnitine palmitoyltransferase 1A, carnitine palmitoyltransferase 2, and acyl-coenzyme A oxidase 1, palmitoyl) were attenuated in FABP1 T94A hepatocytes. Although the phenotype of FABP1 T94A variant human hepatocytes exhibits some similarities to that of FABP1-null or PPAR-α-null hepatocytes and mice, expression of FABP1 T94A variant did not abolish or reduce ligand binding. Thus the FABP1 T94A variant represents an altered/reduced function mutation resulting in TG accumulation.

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24

Feng, Qin, Xiao-jun Gou, Sheng-xi Meng, Cheng Huang, Yu-quan Zhang, Ya-jun Tang, Wen-jing Wang, Lin Xu, Jing-hua Peng, and Yi-yang Hu. "Qushi Huayu Decoction Inhibits Hepatic Lipid Accumulation by Activating AMP-Activated Protein KinaseIn VivoandIn Vitro." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/184358.

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Qushi Huayu Decoction (QHD), a Chinese herbal formula, has been proven effective on alleviating nonalcoholic fatty liver disease (NAFLD) in human and rats. The present study was conducted to investigate whether QHD could inhibit hepatic lipid accumulation by activating AMP-activated protein kinase (AMPK)in vivoandin vitro. Nonalcoholic fatty liver (NAFL) model was duplicated with high-fat diet in rats and with free fatty acid (FFA) in L02 cells. Inin vivoexperimental condition, QHD significantly decreased the accumulation of fatty droplets in livers, lowered low-density lipoprotein cholesterol (LDL-c), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels in serum. Moreover, QHD supplementation reversed the HFD-induced decrease in the phosphorylation levels of AMPK and acetyl-CoA carboxylase (ACC) and decreased hepatic nuclear protein expression of sterol regulatory element-binding protein-1 (SREBP-1) and carbohydrate-responsive element-binding protein (ChREBP) in the liver. Inin vitro, QHD-containing serum decreased the cellular TG content and alleviated the accumulation of fatty droplets in L02 cells. QHD supplementation reversed the FFA-induced decrease in the phosphorylation levels of AMPK and ACC and decreased the hepatic nuclear protein expression of SREBP-1 and ChREBP. Overall results suggest that QHD has significant effect on inhibiting hepatic lipid accumulation via AMPK pathwayin vivoandin vitro.

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25

Mann, Madison M., James D. Tang, and Bryan W. Berger. "Engineering human liver fatty acid binding protein for detection of poly‐ and perfluoroalkyl substances." Biotechnology and Bioengineering 119, no. 2 (November 9, 2021): 513–22. http://dx.doi.org/10.1002/bit.27981.

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26

Suzuki, Toshimitsu, and Teruo Ono. "ONTOGENY OF HEPATIC FATTY ACID-BINDING PROTEIN IMMUNOREACTIVITY IN HUMAN LIVER and INTESTINAL TRACT." Pathology International 38, no. 8 (August 1988): 979–87. http://dx.doi.org/10.1111/j.1440-1827.1988.tb02370.x.

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27

Wolfrum, Christian, Torsten Börchers, James C. Sacchettini, and Friedrich Spener. "Binding of Fatty Acids and Peroxisome Proliferators to Orthologous Fatty Acid Binding Proteins from Human, Murine, and Bovine Liver†." Biochemistry 39, no. 6 (February 2000): 1469–74. http://dx.doi.org/10.1021/bi991638u.

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28

Wolfrum, Christian, Torsten Börchers, James C. Sacchettini, and Friedrich Spener. "Binding of Fatty Acids and Peroxisome Proliferators to Orthologous Fatty Acid Binding Proteins from Human, Murine, and Bovine Liver,." Biochemistry 39, no. 46 (November 2000): 14363. http://dx.doi.org/10.1021/bi0051187.

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29

Kawamura, Tetsuo, Ryuzo Kanno, Hiroshi Fujii, and Toshimitsu Suzuki. "Expression of Liver-Type Fatty-Acid-Binding Protein, Fatty Acid Synthase and Vascular Endothelial Growth Factor in Human Lung Carcinoma." Pathobiology 72, no. 5 (2005): 233–40. http://dx.doi.org/10.1159/000089417.

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30

Yang, Jui-Ting, Yu-Jen Chen, Chao-Wei Huang, Ya-Chin Wang, Harry J. Mersmann, Pei-Hwa Wang, and Shih-Torng Ding. "Docosahexaenoic Acid Suppresses Expression of Adipogenic Tetranectin through Sterol Regulatory Element-Binding Protein and Forkhead Box O Protein in Pigs." Nutrients 13, no. 7 (July 5, 2021): 2315. http://dx.doi.org/10.3390/nu13072315.

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Tetranectin (TN), a plasminogen-binding protein originally involved in fibrinolysis and bone formation, was later identified as a secreted adipokine from human and rat adipocytes and positively correlated with adipogenesis and lipid metabolism in adipocytes. To elucidate the nutritional regulation of adipogenic TN from diets containing different sources of fatty acids (saturated, n-6, n-3) in adipocytes, we cloned the coding region of porcine TN from a cDNA library and analyzed tissue expressions in weaned piglets fed with 2% soybean oil (SB, enriched in n-6 fatty acids), docosahexaenoic acid oil (DHA, an n-3 fatty acid) or beef tallow (BT, enriched in saturated and n-9 fatty acids) for 30 d. Compared with tissues in the BT- or SB-fed group, expression of TN was reduced in the adipose, liver and lung tissues from the DHA-fed group, accompanied with lowered plasma levels of triglycerides and cholesterols. This in vivo reduction was also confirmed in porcine primary differentiated adipocytes supplemented with DHA in vitro. Then, promoter analysis was performed. A 1956-bp putative porcine TN promoter was cloned and transcription binding sites for sterol regulatory-element binding protein (SREBP)-1c or forkhead box O proteins (FoxO) were predicted on the TN promoter. Mutating binding sites on porcine TN promoters showed that transcriptional suppression of TN by DHA on promoter activity was dependent on specific response elements for SREBP-1c or FoxO. The inhibited luciferase promoter activity by DHA on the TN promoter coincides with reduced gene expression of TN, SREBP-1c, and FoxO1 in human embryonic kidney HEK293T cells supplemented with DHA. To conclude, our current study demonstrated that the adipogenic TN was negatively regulated by nutritional modulation of DHA both in pigs in vivo and in humans/pigs in vitro. The transcriptional suppression by DHA on TN expression was partly through SREBP-1c or FoxO. Therefore, down-regulation of adipogenic tetranectin associated with fibrinolysis and adipogenesis may contribute to the beneficial effects of DHA on ameliorating obesity-induced metabolic syndromes such as atherosclerosis and adipose dysfunctions.

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31

Ozcan, Filiz, Halide Akbas, Ebru Kirac, Gultekin Suleymanlar, Gultekin Yucel, and Mutay Aslan. "Mass Spectrometric Quantification of Urinary Human Liver Fatty Acid Binding Protein in Renal Transplant Recipients." Free Radical Biology and Medicine 87 (October 2015): S119. http://dx.doi.org/10.1016/j.freeradbiomed.2015.10.311.

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32

Ozcan, Filiz, Halide Akbas, Ebru Kırac, Gultekin Suleymanlar, Mutay Aslan, and Gultekin Yucel. "Mass spectrometric quantification of urinary human liver fatty acid binding protein in renal transplant recipients." Rapid Communications in Mass Spectrometry 30, no. 5 (February 1, 2016): 603–10. http://dx.doi.org/10.1002/rcm.7474.

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33

Rowland, Andrew, David Hallifax, Matthew R. Nussio, Joseph G. Shapter, Peter I. Mackenzie, J. Brian Houston, Kathleen M. Knights, and John O. Miners. "Characterization of the comparative drug binding to intra- (liver fatty acid binding protein) and extra- (human serum albumin) cellular proteins." Xenobiotica 45, no. 10 (March 24, 2015): 847–57. http://dx.doi.org/10.3109/00498254.2015.1021403.

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34

Figueroa-Santiago, Olgary, and Ana M. Espino. "Fasciola hepatica Fatty Acid Binding Protein Induces the Alternative Activation of Human Macrophages." Infection and Immunity 82, no. 12 (September 15, 2014): 5005–12. http://dx.doi.org/10.1128/iai.02541-14.

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ABSTRACTThe liver flukeFasciola hepaticais a highly evolved parasite that uses sophisticated mechanisms to evade the host immune response. The immunosuppressive capabilities of the parasite have been associated with antigens secreted through the parasite's tegument, called excretory-secretory products (ESPs). Proteomic studies have identified the fatty acid binding protein (FABP) as one of molecules present in the parasite ESPs. Although FABP has been investigated for potential use in the development of vaccines against fascioliasis, its direct interaction with cells of immune system has not been studied. In this study, FABP was purified in native form from soluble extracts ofF. hepaticaadult flukes using a combination of molecular sieving chromatography and preparative isoelectric focusing. The immunological effect of the purified protein, termed Fh12, was assayedin vitrousing monocyte-derived macrophages (MDM) obtained from healthy human donors. Results from the assay indicate that Fh12 produced a significantly increased arginase expression and activity and induced the expression of chitinase-3-like protein (CHI3L1). The assay also showed that Fh12 downregulated the production of nitric oxide (NO) and the expression of nitric oxide synthase (NOS2). This indicates that Fh12 induced the production of alternatively activated macrophages (AAMϕ). The results also demonstrated the ability of Fh12 to downregulate the secretion of the proinflammatory and inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-12 (IL-12), and IL-1βB, even after stimulation with lipopolysaccharide (LPS), as well as its ability to stimulate the overexpression of IL-10. These results suggest a potent anti-inflammatory role for Fh12, which could occur via targeting of Toll-like receptor 4 (TLR4).

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35

Suzuki, T., M. Hitomi, and T. Ono. "Immunohistochemical distribution of hepatic fatty acid-binding protein in rat and human alimentary tract." Journal of Histochemistry & Cytochemistry 36, no. 4 (April 1988): 349–57. http://dx.doi.org/10.1177/36.4.3346538.

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Tissues from rat and human alimentary tract were immunostained with rabbit antibodies to fatty acid-binding protein (FABP) isolated from rat liver, since the precise immunohistochemical localization of the protein in gut has not been determined. The results obtained indicated that FABP immunoreactivity was found almost exclusively in intestinal absorptive cells, the sole exception being its presence in the cytoplasm of a few goblet cells. In small bowel, FABP-positive cells were most often found in the upper and middle segments, and less frequently in the lower to terminal portion. Immunoreactive cells were also found in large bowel of rat and human, but with differing patterns of distribution. In rat, positive cells were found mainly in the lower portion of the large intestine, whereas in human positive cells were present in all portions. Immunoreactive cells were detected in rat and human cecum, in the upper half of human rectum, and in human vermiform appendix. No such cells were found in esophageal and nonmetaplastic gastric mucosa or in pancreatic tissue, whereas they were present in great numbers in metaplastic gastric mucosa. The results of this study therefore suggest that FABP is a useful marker for research into the physiology or pathology of absorptive cells in the gastrointestinal tracts of both species.

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36

Fatoki, Toluwase Hezekiah, Cecilia O. Akintayo, and Omodele Ibraheem. "Bioinformatics exploration of olive oil: molecular targets and properties of major bioactive constituents." OCL 28 (2021): 36. http://dx.doi.org/10.1051/ocl/2021024.

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Olive oil possesses medicinal properties which include antimicrobial, antioxidant and anti-inflammatory, anti-diabetes, and anti-cardiovascular diseases. Oleic acid is the most abundant (95%) constituent of olive oil and others include linoleic acid, oleuropein, oleanolic acid, maslinic acid, melatonin, and others. The objective of this study is to predict the molecular targets and properties of key bioactive components of olive oil in human. Bioinformatics methods, which involved pharmacokinetics prediction, target prediction and gene network analyses, were used. The results showed that oleic acid has similar targets with linoleic acid, and showed significant probability of binding to several targets such as fatty acid-binding proteins in the adipose, epidermal, liver and muscle as well as alpha, delta and gamma peroxisome proliferator-activated receptors (PPARs). Carbonic anhydrase showed to be the only significant target of tyrosol, while protein-tyrosine phosphatase 1B, and CD81 antigen were targeted by maslinic acid and oleanolic acid. This study has applauded oleic acid, linoleic acid and tyrosol as olive oil bioactive constituents that have several potential pharmacological effects in humans that modulate several enzymes, receptors and transcription factors. The future work will be to investigate the effects of oleic acid on fatty acid-binding proteins and telomerase reverse transcriptase; melatonin on quinone reductase 2; tyrosol on carbonic anhydrase II; maslinic acid and oleanolic acid on protein-tyrosine phosphatase 1B.

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Ushio, Masateru, Yoshihiko Nishio, Osamu Sekine, Yoshio Nagai, Yasuhiro Maeno, Satoshi Ugi, Takeshi Yoshizaki, et al. "Ezetimibe prevents hepatic steatosis induced by a high-fat but not a high-fructose diet." American Journal of Physiology-Endocrinology and Metabolism 305, no. 2 (July 15, 2013): E293—E304. http://dx.doi.org/10.1152/ajpendo.00442.2012.

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Nonalcoholic fatty liver disease is the most frequent liver disease. Ezetimibe, an inhibitor of intestinal cholesterol absorption, has been reported to ameliorate hepatic steatosis in human and animal models. To explore how ezetimibe reduces hepatic steatosis, we investigated the effects of ezetimibe on the expression of lipogenic enzymes and intestinal lipid metabolism in mice fed a high-fat or a high-fructose diet. CBA/JN mice were fed a high-fat diet or a high-fructose diet for 8 wk with or without ezetimibe. High-fat diet induced hepatic steatosis accompanied by hyperinsulinemia. Treatment with ezetimibe reduced hepatic steatosis, insulin levels, and glucose production from pyruvate in mice fed the high-fat diet, suggesting a reduction of insulin resistance in the liver. In the intestinal analysis, ezetimibe reduced the expression of fatty acid transfer protein-4 and apoB-48 in mice fed the high-fat diet. However, treatment with ezetimibe did not prevent hepatic steatosis, hyperinsulinemia, and intestinal apoB-48 expression in mice fed the high-fructose diet. Ezetimibe decreased liver X receptor-α binding to the sterol regulatory element-binding protein-1c promoter but not expression of carbohydrate response element-binding protein and fatty acid synthase in mice fed the high-fructose diet, suggesting that ezetimibe did not reduce hepatic lipogenesis induced by the high-fructose diet. Elevation of hepatic and intestinal lipogenesis in mice fed a high-fructose diet may partly explain the differences in the effect of ezetimibe.

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Ichikawa, Daisuke, Atsuko Kamijo-Ikemori, Takeshi Sugaya, Yugo Shibagaki, Takashi Yasuda, Seiko Hoshino, Kimie Katayama, Junko Igarashi-Migitaka, Kazuaki Hirata, and Kenjiro Kimura. "Human liver-type fatty acid–binding protein protects against tubulointerstitial injury in aldosterone-induced renal injury." American Journal of Physiology-Renal Physiology 308, no. 2 (January 15, 2015): F114—F121. http://dx.doi.org/10.1152/ajprenal.00469.2014.

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To demonstrate the renoprotective function of human liver-type fatty acid–binding protein (hL-FABP) expressed in proximal tubules in aldosterone (Aldo)-induced renal injury, hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice received systemic Aldo infusions (Tg-Aldo and WT-Aldo, respectively) were given 1% NaCl water for 28 days. In this model, elevation of systolic blood pressure, monocyte chemoattractant protein-1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed. Elevation of systolic blood pressure did not differ in WT-Aldo vs. Tg-Aldo animals, however, renal injury was suppressed in Tg-Aldo compared with WT-Aldo mice. Dihydroethidium fluorescence was used to evaluate reactive oxidative stress, which was suppressed in Tg-Aldo compared with WT-Aldo mice. Gene expression of angiotensinogen in the kidney was upregulated, and excretion of urinary angiotensinogen was increased in WT-Aldo mice. This exacerbation was suppressed in Tg-Aldo mice. Expression of hL-FABP was upregulated in proximal tubules of Tg-Aldo mice. Urinary excretion of hL-FABP was significantly greater in Tg-Aldo than in Tg-control mice. In conclusion, hL-FABP ameliorated the tubulointerstitial damage in Aldo-induced renal injury via reducing oxidative stress and suppressing activation of the intrarenal renin-angiotensin system.

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Zhang, Lianying, Xiao-Min Ren, and Liang-Hong Guo. "Structure-Based Investigation on the Interaction of Perfluorinated Compounds with Human Liver Fatty Acid Binding Protein." Environmental Science & Technology 47, no. 19 (September 20, 2013): 11293–301. http://dx.doi.org/10.1021/es4026722.

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40

Ajmo, Joanne M., Xiaomei Liang, Christopher Q. Rogers, Brandi Pennock, and Min You. "Resveratrol alleviates alcoholic fatty liver in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 4 (October 2008): G833—G842. http://dx.doi.org/10.1152/ajpgi.90358.2008.

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Alcoholic fatty liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of alcoholic liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of fatty acid oxidation and prevented alcoholic liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human alcoholic fatty liver disease.

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Wu, Yun-li, Xian-e. Peng, Dong Wang, Wan-nan Chen, and Xu Lin. "Human liver fatty acid binding protein (hFABP1) gene is regulated by liver-enriched transcription factors HNF3β and C/EBPα." Biochimie 94, no. 2 (February 2012): 384–92. http://dx.doi.org/10.1016/j.biochi.2011.08.006.

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42

PELSERS, Maurice M. A. L., Jan T. LUTGERINK, Frans A. van NIEUWENHOVEN, Narendra N. TANDON, Ger J. van der VUSSE, Jan-Willem ARENDS, Hennie R. HOOGENBOOM, and Jan F. C. GLATZ. "A sensitive immunoassay for rat fatty acid translocase (CD36) using phage antibodies selected on cell transfectants: abundant presence of fatty acid translocase/CD36 in cardiac and red skeletal muscle and up-regulation in diabetes." Biochemical Journal 337, no. 3 (January 25, 1999): 407–14. http://dx.doi.org/10.1042/bj3370407.

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The rat membrane protein fatty acid translocase (FAT), which shows sequence similarity to human CD36 (a membrane protein supposedly involved in a variety of membrane processes), is implicated in the transport of long-chain fatty acids across cellular membranes. To set up an immunoassay for quantification of FAT in different tissues, we isolated a series of anti-FAT antibodies by panning a large naive phage antibody library on FAT-transfected H9c2 cells. All seven different phage antibody fragments isolated reacted specifically with FAT, and most likely recognize the same or closely located immunodominant sites on FAT, as a competitive monoclonal antibody (mAb) (CLB-IV7) completely blocked the binding of all these phage antibodies to cells. A sandwich ELISA was set up using mAb 131.4 (directed against purified CD36 from human platelets) as capture antibody and phage antibodies and anti-phage sera as detector. With this ELISA (sensitivity 0.05 µg/ml), the FAT content in isolated cardiomyocytes was found to be comparable with that of total heart (≈ 3 mg/g of protein), while liver tissue and endothelial cells were below the detection limit (< 0.1 mg of FAT/g of protein). During rat heart development, protein levels of FAT rose from 1.7±0.7 mg/g of protein on the day before birth to 3.6±0.4 mg/g of protein on day 70. Comparing control with streptozotocin-induced diabetic rats, a statistically significant (P< 0.05) 2–4-fold increase of FAT was seen in heart (from 4.2±2.3 to 11.0±5.7 mg/g of protein), soleus (from 0.6±0.1 to 1.4±0.5 mg/g of protein) and extensor digitorum longus (EDL) muscle (from 0.3±0.1 to 1.2±0.8 mg/g of protein). In addition, the FAT contents of each of these muscles were found to be of similar magnitude to the contents of cytoplasmic heart-type fatty-acid-binding protein in both diabetic rats and controls, supporting the suggested roles of these two proteins in cellular fatty acid metabolism. This is the first time phage display technology has been succesfully applied for direct selection, from a large naive antibody library, of antibodies that recognize selected membrane proteins in their natural context.

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Peeters, Roger A., Monique A. P. M. in't Groen, Marielle P. de Moel, Herman T. B. Van Moerkerk, and Jacques H. Veerkamp. "The binding affinity of fatty acid-binding proteins from human, pig and rat liver for different fluorescent fatty acids and other ligands." International Journal of Biochemistry 21, no. 4 (January 1989): 407–18. http://dx.doi.org/10.1016/0020-711x(89)90365-0.

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44

Attal, Neha, Emilio Marrero, Kyle J. Thompson, and Iain H. McKillop. "Role of AMPK-SREBP Signaling in Regulating Fatty Acid Binding-4 (FABP4) Expression following Ethanol Metabolism." Biology 11, no. 11 (November 4, 2022): 1613. http://dx.doi.org/10.3390/biology11111613.

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Fatty acid binding protein-4 (FABP4) is not normally expressed in the liver but is induced in alcohol-dependent liver disease (ALD)). This study sought to identify mechanisms whereby ethanol (EtOH) metabolism alters triglyceride accumulation and FABP4 production. Human hepatoma cells which were stably transfected to express alcohol dehydrogenase (ADH) or cytochrome P4502E1 (CYP2E1) were exposed to EtOH in the absence/presence of inhibitors of ADH (4-methylpyrazole) or CYP2E1 (chlormethiazole). Cells were analyzed for free fatty acid (FFA) content and FABP4 mRNA, then culture medium assayed for FABP4 levels. Cell lysates were analyzed for AMP-activated protein kinase-α (AMPKα), Acetyl-CoA carboxylase (ACC), sterol regulatory element binding protein-1c (SREBP-1c), and Lipin-1β activity and localization in the absence/presence of EtOH and pharmacological inhibitors. CYP2E1-EtOH metabolism led to increased FABP4 mRNA/protein expression and FFA accumulation. Analysis of signaling pathway activity revealed decreased AMPKα activation and increased nuclear-SREBP-1c localization following CYP2E1-EtOH metabolism. The role of AMPKα-SREBP-1c in regulating CYP2E1-EtOH-dependent FFA accumulation and increased FABP4 was confirmed using pharmacological inhibitors and over-expression of AMPKα. Inhibition of ACC or Lipin-1β failed to prevent FFA accumulation or changes in FABP4 mRNA expression or protein secretion. These data suggest that CYP2E1-EtOH metabolism inhibits AMPKα phosphorylation to stimulate FFA accumulation and FABP4 protein secretion via an SREBP-1c dependent mechanism.

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45

Liu, Xiaoying, Anne S. Henkel, Brian E. LeCuyer, Matthew J. Schipma, Kristy A. Anderson, and Richard M. Green. "Hepatocyte X-box binding protein 1 deficiency increases liver injury in mice fed a high-fat/sugar diet." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 12 (December 15, 2015): G965—G974. http://dx.doi.org/10.1152/ajpgi.00132.2015.

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Fatty liver is associated with endoplasmic reticulum stress and activation of the hepatic unfolded protein response (UPR). Reduced hepatic expression of the UPR regulator X-box binding protein 1 spliced (XBP1s) is associated with human nonalcoholic steatohepatitis (NASH), and feeding mice a high-fat diet with fructose/sucrose causes progressive, fibrosing steatohepatitis. This study examines the role of XBP1 in nonalcoholic fatty liver injury and fatty acid-induced cell injury. Hepatocyte-specific Xbp1-deficient ( Xbp1−/−) mice were fed a high-fat/sugar (HFS) diet for up to 16 wk. HFS-fed Xbp1−/− mice exhibited higher serum alanine aminotransferase levels compared with Xbp1fl/fl controls. RNA sequencing and Gene Ontogeny pathway analysis of hepatic mRNA revealed that apoptotic process, inflammatory response, and extracellular matrix structural constituent pathways had enhanced activation in HFS-fed Xbp1−/− mice. Liver histology demonstrated enhanced injury and fibrosis but less steatosis in the HFS-fed Xbp1−/− mice. Hepatic Col1a1 and Tgfβ1 gene expression, as well as Chop and phosphorylated JNK (p-JNK), were increased in Xbp1−/− compared with Xbp1fl/fl mice after HFS feeding. In vitro, stable XBP1-knockdown Huh7 cells (Huh7-KD) and scramble control cells (Huh7-SCR) were generated and treated with palmitic acid (PA) for 24 h. PA-treated Huh7-KD cells had increased cytotoxicity measured by lactate dehydrogenase release, apoptotic nuclei, and caspase3/7 activity assays compared with Huh7-SCR cells. CHOP and p-JNK expression was also increased in Huh7-KD cells following PA treatment. In conclusion, loss of XBP1 enhances injury in both in vivo and in vitro models of fatty liver injury. We speculate that hepatic XBP1 plays an important protective role in pathogenesis of NASH.

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46

Das, Tanya, Gourisankar Sa, and Manju Mukherjea. "Human fetal liver fatty acid binding proteins. Role on glucose-6-phosphate dehydrogenase activity." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1002, no. 2 (April 1989): 164–72. http://dx.doi.org/10.1016/0005-2760(89)90283-x.

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47

Hansbrough, J. R., D. M. Lublin, K. A. Roth, E. A. Birkenmeier, and J. I. Gordon. "Expression of a liver fatty acid binding protein/human decay-accelerating factor/HLA-B44 chimeric gene in transgenic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 6 (June 1, 1991): G929—G939. http://dx.doi.org/10.1152/ajpgi.1991.260.6.g929.

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The intestinal epithelium is characterized by the rapid and continuous renewal of its four principal cell types and by its ability to establish and maintain remarkably complex spatial differentiation along its crypt-to-villus and duodenal-to-colonic axes. We have previously used transgenic mice containing liver fatty acid binding protein/human growth hormone (L-FABP/hGH) fusion genes to analyze the molecular mechanisms responsible for encoding positional information in this epithelium. Because these studies could not distinguish whether cis-acting sequences in the L-FABP promoter or hGH structural gene were responsible for the observed cellular and regional patterns of transgene transcription in the gut, a second model fusion gene has now been constructed. It consists of nucleotides -596 to +21 of rat L-FABP linked to a cDNA encoding a chimeric protein, human decay-accelerating factor (DAF, minus the site of attachment of its COOH-terminal glycophospholipid anchor), coupled to the transmembrane (TM) and cytoplasmic domains of human HLA-B44. RNA blot hybridization and immunocytochemical analyses revealed that the cell-specific and region-specific expressions of DAF-TM and hGH in adult mice appear identical along both axes of the gut, indicating that cis-acting elements contained within the 5' nontranscribed region of the L-FABP gene rather than in the reporter are largely responsible for these observed patterns of transgene expression. Unlike pre-hGH, a prototypical secreted protein, DAF-TM is a membrane protein. The ability to direct its expression along the length of both axes of the gut provides an opportunity to analyze in vivo the sorting pathways of membrane-associated proteins in normal epithelial cells as a function of their location and differentiation. Light microscopic studies indicate that DAF-TM is targeted to the basolateral and apical surfaces of villus-associated enterocytes.

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Martin, Gregory G., Avery L. McIntosh, Huan Huang, Shipra Gupta, Barbara P. Atshaves, Kerstin K. Landrock, Danilo Landrock, Ann B. Kier, and Friedhelm Schroeder. "The Human Liver Fatty Acid Binding Protein T94A Variant Alters the Structure, Stability, and Interaction with Fibrates." Biochemistry 52, no. 51 (December 10, 2013): 9347–57. http://dx.doi.org/10.1021/bi401014k.

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49

Sheng, Nan, Ruina Cui, Jinghua Wang, Yong Guo, Jianshe Wang, and Jiayin Dai. "Cytotoxicity of novel fluorinated alternatives to long-chain perfluoroalkyl substances to human liver cell line and their binding capacity to human liver fatty acid binding protein." Archives of Toxicology 92, no. 1 (September 1, 2017): 359–69. http://dx.doi.org/10.1007/s00204-017-2055-1.

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50

Oem, Jae-Ku, Candice Jackel-Cram, Yi-Ping Li, Yan Zhou, Jin Zhong, Hitoshi Shimano, Lorne A. Babiuk, and Qiang Liu. "Activation of sterol regulatory element-binding protein 1c and fatty acid synthase transcription by hepatitis C virus non-structural protein 2." Journal of General Virology 89, no. 5 (May 1, 2008): 1225–30. http://dx.doi.org/10.1099/vir.0.83491-0.

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Transcriptional factor sterol regulatory element-binding protein 1c (SREBP-1c) activates the transcription of lipogenic genes, including fatty acid synthase (FAS). Hepatitis C virus (HCV) infection is often associated with lipid accumulation within the liver, known as steatosis in the clinic. The molecular mechanisms of HCV-associated steatosis are not well characterized. Here, we showed that HCV non-structural protein 2 (NS2) activated SREBP-1c transcription in human hepatic Huh-7 cells as measured by using a human SREBP-1c promoter–luciferase reporter plasmid. We further showed that sterol regulatory element (SRE) and liver X receptor element (LXRE) in the SREBP-1c promoter were involved in SREBP-1c activation by HCV NS2. Furthermore, expression of HCV NS2 resulted in the upregulation of FAS transcription. We also showed that FAS upregulation by HCV NS2 was SREBP-1-dependent since deleting the SRE sequence in a FAS promoter and expressing a dominant-negative SREBP-1 abrogated FAS promoter upregulation by HCV NS2. Taken together, our results suggest that HCV NS2 can upregulate the transcription of SREBP-1c and FAS, and thus is probably a contributing factor for HCV-associated steatosis.

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