Corrigendum to “Hepatic fatty acid uptake is regulated by the sphingolipid acyl chain length” [Mol. Cell Biol. Lipids 1841(12) (2014) 1754–1766]

Phosphatidates (PA or phosphatidic acid) were shown to have mitogenic properties, including the stimulation of DNA synthesis and calcium mobilization in C3H/10T1/2 cells. Their continuous presence for a minimum of 7 h induced DNA synthesis with kinetics similar to that observed when 10% fetal bovine serum was used as a mitogen. PAs with long chain saturated fatty acid moieties were more mitogenic, in a dose-dependent fashion, than PAs with short saturated or unsaturated fatty acid moieties. When compared with lysostearoyl-PA (LSPA), distearoyl-PA (DSPA) was as potent with respect to the induction of DNA synthesis. Lysooleoyl-PA (LOPA) was slightly more potent than dioleoyl-PA (DOPA), but much weaker than DSPA and LSPA. Preincubation with dilauroyl-PA (DLPA) reduces the mitogenic effect of DSPA by 85%. The pattern of mitogenic inhibition suggests that a chain-length-independent, yet PA-specific, mechanism is involved. Both DSPA and DLPA are equally taken up by the cells after 30 min. LOPA, but not LSPA, produced a large calcium transient (1.3 microM), which we found to be derived from intracellular sources. DSPA, the most mitogenic PA tested, produced a weaker transient (0.6 microM). Interestingly, LSPA did not produce any detectable calcium transient. These results suggest that the chain-length-specific step in the signaling mechanism of PA occurs after the initial chain-length-independent partitioning and/or binding to the membrane and that the induction of DNA synthesis is not related to the observed calcium transients.

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Fasting‐induced liver GADD 45β restrains hepatic fatty acid uptake and improves metabolic health

EMBO Molecular Medicine ◽

10.15252/emmm.201505801 ◽

2016 ◽

Vol 8 (6) ◽

pp. 654-669 ◽

Cited By ~ 15

Author(s):

Jessica Fuhrmeister ◽

Annika Zota ◽

Tjeerd P Sijmonsma ◽

Oksana Seibert ◽

Şahika Cıngır ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Uptake ◽

Metabolic Health ◽

Acid Uptake ◽

Hepatic Fatty Acid

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Increased Hepatic Fatty Acid Uptake and Esterification Contribute to Tetracycline-Induced Steatosis in Mice

Toxicological Sciences ◽

10.1093/toxsci/kfv049 ◽

2015 ◽

Vol 145 (2) ◽

pp. 273-282 ◽

Cited By ~ 18

Author(s):

You-Jin Choi ◽

Chae-Hyeon Lee ◽

Kang-Yo Lee ◽

Seung-Hwan Jung ◽

Byung-Hoon Lee

Keyword(s):

Fatty Acid ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Hepatic Fatty Acid

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Faculty Opinions recommendation of Specific bile acids inhibit hepatic fatty acid uptake in mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717960248.793463325 ◽

2012 ◽

Author(s):

Bruno Stieger

Keyword(s):

Fatty Acid ◽

Bile Acids ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Hepatic Fatty Acid

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Mechanism of Hepatic Fatty Acid Uptake

Assessment and Management of Hepatobiliary Disease ◽

10.1007/978-3-642-72631-6_3 ◽

1987 ◽

pp. 13-22

Author(s):

Wolfgang Stremmel ◽

Paul D. Berk

Keyword(s):

Fatty Acid ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Hepatic Fatty Acid

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The elongation of exogenous fatty acids and the control of phospholipid acyl chain length in Micrococcus cryophilus

Biochemical Journal ◽

10.1042/bj1880585 ◽

1980 ◽

Vol 188 (3) ◽

pp. 585-592 ◽

Cited By ~ 8

Author(s):

S P Sandercock ◽

N J Russell

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Chain Length ◽

De Novo ◽

Acyl Chain ◽

Psychrophilic Bacterium ◽

Fatty Acid Elongation ◽

Acyl Chain Length ◽

Acyl Chains ◽

Phospholipid Acyl Chain

The synthesis of fatty acids de novo from acetate and the elongation of exogenous satuated fatty acids (C12-C18) by the psychrophilic bacterium Micrococcus cryophilus (A.T.C.C. 15174) grown at 1 or 20 degrees C was investigated. M. cryophilus normally contains only C16 and C18 acyl chains in its phospholipids, and the C18/C16 ratio is altered by changes in growth temperature. The bacterium was shown to regulate strictly its phospholipid acyl chain length and to be capable of directly elongating myristate and palmitate, and possibly laurate, to a mixture of C16 and C18 acyl chains. Retroconversion of stearate into palmitate also occurred. Fatty acid elongation could be distinguished from fatty acid synthesis de novo by the greater sensitivity of fatty acid elongation to inhibition by NaAsO2 under conditions when the supply of ATP and reduced nicotinamide nucleotides was not limiting. It is suggested that phospholipid acyl chain length may be controlled by a membrane-bound elongase enzyme, which interconverts C16 and C18 fatty acids via a C14 intermediate; the activity of the enzyme could be regulated by membrane lipid fluidity.

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FATP2 is a hepatic fatty acid transporter and peroxisomal very long-chain acyl-CoA synthetase

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00226.2010 ◽

2010 ◽

Vol 299 (3) ◽

pp. E384-E393 ◽

Cited By ~ 96

Author(s):

Alaric Falcon ◽

Holger Doege ◽

Amy Fluitt ◽

Bernice Tsang ◽

Nicki Watson ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Uptake ◽

Fatty Acid Transport ◽

Acid Uptake ◽

Peroxisomal Enzyme ◽

Multifunctional Protein ◽

Hepatic Fatty Acid ◽

Chain Acyl ◽

Lcfa Uptake ◽

Long Chain

Fatty acid transport protein (FATP)2, a member of the FATP family of fatty acid uptake mediators, has independently been identified as a hepatic peroxisomal very long-chain acyl-CoA synthetase (VLACS). Here we address whether FATP2 is 1) a peroxisomal enzyme, 2) a plasma membrane-associated long-chain fatty acid (LCFA) transporter, or 3) a multifunctional protein. We found that, in mouse livers, only a minor fraction of FATP2 localizes to peroxisomes, where it contributes to approximately half of the peroxisomal VLACS activity. However, total hepatic (V)LACS activity was not significantly affected by loss of FATP2, while LCFA uptake was reduced by 40%, indicating a more prominent role in hepatic LCFA uptake. This suggests FATP2 as a potential target for a therapeutic intervention of hepatosteatosis. Adeno-associated virus 8-based short hairpin RNA expression vectors were used to achieve liver-specific FATP2 knockdown, which significantly reduced hepatosteatosis in the face of continued high-fat feeding, concomitant with improvements in liver physiology, fasting glucose, and insulin levels. Based on our findings, we propose a model in which FATP2 is a multifunctional protein that shows subcellular localization-dependent activity and is a major contributor to peroxisomal (V)LACS activity and hepatic fatty acid uptake, suggesting FATP2 as a potential novel target for the treatment of nonalcoholic fatty liver disease.

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A Model Construction of Starvation Induces Hepatic Steatosis and Transcriptome Analysis in Zebrafish Larvae

Biology ◽

10.3390/biology10020092 ◽

2021 ◽

Vol 10 (2) ◽

pp. 92

Author(s):

Hao Xu ◽

Yu Jiang ◽

Xiao-Min Miao ◽

Yi-Xi Tao ◽

Lang Xie ◽

...

Keyword(s):

Fatty Acid ◽

Hepatic Steatosis ◽

Fatty Acid Metabolism ◽

Transcriptome Analysis ◽

Acid Metabolism ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Alcoholic Fatty Liver ◽

Zebrafish Larvae ◽

Hepatic Fatty Acid

Hepatic steatosis caused by starvation, resulting in non-alcoholic fatty liver disease (NAFLD), has been a research topic of human clinical and animal experiments. To understand the molecular mechanisms underlying the triggering of abnormal liver metabolism by starvation, thus inducing hepatic lipid accumulation, we used zebrafish larvae to establish a starvation-induced hepatic steatosis model and conducted comparative transcriptome analysis by RNA-seq. We demonstrated that the incidence of larvae steatosis is positively correlated with starvation time. Under starvation conditions, the fatty acid transporter (slc27a2a and slc27a6-like) and fatty acid translocase (cd36) were up-regulated significantly to promote extrahepatic fatty acid uptake. Meanwhile, starvation inhibits the hepatic fatty acid metabolism pathway but activates the de novo lipogenesis pathway to a certain extent. More importantly, we detected that the expression of numerous apolipoprotein genes was downregulated and the secretion of very low density lipoprotein (VLDL) was inhibited significantly. These data suggest that starvation induces hepatic steatosis by promoting extrahepatic fatty acid uptake and lipogenesis, and inhibits hepatic fatty acid metabolism and lipid transport. Furthermore, we found that starvation-induced hepatic steatosis in zebrafish larvae can be rescued by targeting the knockout cd36 gene. In summary, these findings will help us understand the pathogenesis of starvation-induced NAFLD and provide important theoretical evidence that cd36 could serve as a potential target for the treatment of NAFLD.

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Studies on the uptake of fatty acids by brush border membranes of the rabbit intestine

Canadian Journal of Biochemistry and Cell Biology ◽

10.1139/o85-036 ◽

1985 ◽

Vol 63 (4) ◽

pp. 249-256 ◽

Cited By ~ 13

Author(s):

P. Proulx ◽

H. Aubry ◽

I. Brglez ◽

D. G. Williamson

Keyword(s):

Fatty Acids ◽

Oleic Acid ◽

Fatty Acid ◽

Palmitic Acid ◽

Bile Salt ◽

Chain Length ◽

Brush Border ◽

Fatty Acid Uptake ◽

Acid Uptake ◽

Egg Lecithin

Initial studies revealed that the uptake of palmitic acid and oleic acid into brush border membranes was similar when these were isolated from either whole small intestine, jejunum, or ileum. The uptake of these fatty acids was somewhat lower with membranes obtained from duodenum. Subsequent studies, all with membranes obtained from whole intestine, indicated an increase in binding with chain length of fatty acid of up to 16 carbons. Unsaturation decreased this uptake somewhat. Taurocholate and 1-palmitoyl lysolecithin had a moderate stimulatory effect on the binding of oleic acid and palmitic acid at concentrations of 10 and 0.5 mM, respectively, and inhibited at higher concentrations. Addition of 1.4 mM egg lecithin to the fatty acid – bile salt micelles, such that the lecithin – bile salt ratio was 0.2, decreased the uptake of fatty acids generally, but did not significantly affect the pattern of binding by membrane fractions isolated from different segments nor did it change the pattern of labelling when fatty acid chain length and unsaturation were varied. At lower concentrations, egg lecithin had little effect on the uptake of oleic acid, whereas dipalmitoyl phosphatidylcholine stimulated binding of both palmitic acid and oleic acid over the entire range of concentrations tested. Preincubation of the membranes with this saturated phospholipid stimulated the uptake of oleic acid, and addition of this choline lipid to the oleic acid – bile salt containing micelles did not substantially enhance fatty acid uptake in lipid-treated membranes. The binding of fatty acid was very rapid either in the presence or the absence of Ca2+, such that even in zero-time controls essentially equilibrium bindings were obtained. The presence of Ca2+ stimulated the incorporation substantially. The results as a whole indicate that fatty acid uptake into brush border membrane is very responsive to a variety of conditions which could prevail in the gut during the absorption process.

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