scholarly journals Ethanolamine Phospholipid Metabolism in Myelinating Rat Brain

1972 ◽  
Vol 25 (1) ◽  
pp. 125 ◽  
Author(s):  
SJ Wysocki ◽  
W Segal
Keyword(s):  
Fatty Acid ◽  
Palmitic Acid ◽  
Aldehyde Dehydrogenase ◽  
Phospholipid Metabolism ◽  
Intracerebral Injection ◽  
Fatty Acid Chain ◽  
Ethanolamine Plasmalogen ◽  
Old Rats ◽  
Ethanolamine Phospholipid

3H-1abelled ethanolamine phospholipids were isolated from the brains of 13-day-old rats after intracerebral injection of [9,1O-3H]palmitic acid. Groups of rats of the same age were injected intracerebrally with preparations derived from the whole labelled fraction, the ethanolamine plasmalogen-depleted fraction, or [14C]palmitic acid. A study of the distribution of radioactivity in phospholipids and sphingolipids, 2 hr after injection, indicates that the alkenyl chains of ethanolamine plasmalogen are effective precursors of the acyl groups of sphingomyelin and cere-broside. This role of plasmalogen is discussed in terms of the properties and distribu-tion of plasmalogenase, aldehyde dehydrogenase, and fatty acid chain-lengthening enzymes in brain.

The Role of Dietary Lipid in the Regulation of Unconjugated Hyperbilirubinaemia in Gunn Rats

1979 ◽  
Vol 57 (4) ◽  
pp. 327-337 ◽  
Author(s):  
J. L. Gollan ◽  
D. R. Hole ◽  
Barbara H. Billing
Keyword(s):  
Fatty Acid ◽  
Plasma Concentrations ◽  
Dietary Lipid ◽  
Normal Diet ◽  
Degree Of Saturation ◽  
Bilirubin Concentration ◽  
Fatty Acid Chain ◽  
Gunn Rats ◽  
Plasma Bilirubin

1. The purpose of this study was to characterize the mechanisms of diet-induced hyperbilirubinaemia in Gunn rats with emphasis on the role of lipids, and to examine their relationship with regard to fasting hyperbilirubinaemia. 2. A lipid-free normocaloric diet produced a threefold increase in plasma bilirubin concentration (baseline 109.4 μmol/l), which was maximal by 10 days and thereafter remained constant. The level of hyperbilirubinaemia attained was not influenced by fasting or phenobarbitone, and returned to baseline concentration within 10 days of resuming a normal diet. 3. Determination of hepatic bilirubin showed that the magnitude of the hepatic bilirubin pool was increased by the lipid-free diet but was unchanged by fasting. Hepatic ligandin concentrations were comparable in fasted Gunn rats and those fed normal or lipid-free diets, although total hepatic ligandin was reduced in the fasted animals. 4. The hyperbilirubinaemic effect of the lipid-free diet was largely reversed by the inclusion of 10% lipid in the diet and was affected to a lesser extent by 5% lipid. Similar reductions in plasma bilirubin concentration were observed with a variety of other lipids (10%), regardless of their fatty acid chain length or degree of saturation. 5. In fasting animals a direct correlation was observed between plasma bilirubin and free fatty acid concentrations and insulin levels were greatly depressed, whereas in those fed on the lipid-free diet no significant changes were evident in plasma concentrations of free fatty acids or insulin. 6. Plasma bilirubin concentration was unrelated to alterations in plasma triglycerides produced by the administration of clofibrate. However, an unexplained decrease in plasma bilirubin (40%) without a significant change in triglycerides was noted when clofibrate was added to the lipid-free diet. 7. Analysis of kinetic data obtained from [14C]bilirubin clearance studies revealed that hyperbilirubinaemia associated with the lipid-free diet reflected a marked reduction (60%) in plasma clearance with no change in bilirubin turnover. This was accompanied by a relative redistribution of bilirubin from the extravascular pool to the plasma pool. 8. Although these studies indicate that fasting and the withdrawal of dietary lipid have some similar effects on bilirubin metabolism, it seems likely that different mechanisms are responsible for the hyperbilirubinaemia.

scholarly journals Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1567
Author(s):  
C. J. Urso ◽  
Heping Zhou
Keyword(s):  
Fatty Acid ◽  
Palmitic Acid ◽  
Critical Role ◽  
Scavenger Receptor ◽  
Neuroblastoma Cells ◽  
Anionic Phospholipids ◽  
N2a Cells ◽  
Diploid Cells ◽  
Long Chain

Elevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of long-chain free fatty acids (FFAs) into cells, serves a fatty acid (FA) sensing function in areas including taste buds and the proximal gut, and acts as a scavenger receptor that binds to many ligands, including FAs, collagen, oxidized low-density lipoproteins, and anionic phospholipids. However, the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells remains unclear. In this study, we examined FA uptake in BSA- and PA-treated N2a cells and investigated the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells. Our data showed that PA treatment promoted FA uptake in N2a cells, and that treatment with sulfo-N-succinimidyl oleate (SSO), a CD36 inhibitor, significantly decreased FA uptake in BSA- and PA-treated N2a cells, and ameliorated PA-induced decrease of cell viability, decrease of diploid cells, and increase of tetraploid cells. We also found that CD36 knockdown significantly decreased FA uptake in both BSA- and PA-treated cells as compared to their corresponding wild-type controls, and dramatically attenuated PA-induced cell cycle defects in N2a cells. Our data suggest that CD36 may play a critical role in FA uptake and PA lipotoxicity in N2a cells. CD36 may therefore represent a regulatory target against pathologies caused by excess FAs.

scholarly journals Fatty acid conjugation enhances potency of antisense oligonucleotides in muscle

2019 ◽  
Vol 47 (12) ◽  
pp. 6029-6044 ◽  
Author(s):  
Thazha P Prakash ◽  
Adam E Mullick ◽  
Richard G Lee ◽  
Jinghua Yu ◽  
Steve T Yeh ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Palmitic Acid ◽  
Binding Affinity ◽  
Chain Length ◽  
Plasma Proteins ◽  
Mouse Muscle ◽  
Muscle Disorders ◽  
Fatty Acid Chain Length ◽  
Fatty Acid Chain ◽  
Muscle Tissues

Abstract Enhancing the functional uptake of antisense oligonucleotide (ASO) in the muscle will be beneficial for developing ASO therapeutics targeting genes expressed in the muscle. We hypothesized that improving albumin binding will facilitate traversal of ASO from the blood compartment to the interstitium of the muscle tissues to enhance ASO functional uptake. We synthesized structurally diverse saturated and unsaturated fatty acid conjugated ASOs with a range of hydrophobicity. The binding affinity of ASO fatty acid conjugates to plasma proteins improved with fatty acid chain length and highest binding affinity was observed with ASO conjugates containing fatty acid chain length from 16 to 22 carbons. The degree of unsaturation or conformation of double bond appears to have no influence on protein binding or activity of ASO fatty acid conjugates. Activity of fatty acid ASO conjugates correlated with the affinity to albumin and the tightest albumin binder exhibited the highest activity improvement in muscle. Palmitic acid conjugation increases ASO plasma Cmax and improved delivery of ASO to interstitial space of mouse muscle. Conjugation of palmitic acid improved potency of DMPK, Cav3, CD36 and Malat-1 ASOs (3- to 7-fold) in mouse muscle. Our approach provides a foundation for developing more effective therapeutic ASOs for muscle disorders.

scholarly journals Role of the stearyl-coenzyme A desaturase 1 gene in regulating palmitic acid tolerance of goose primary hepatocytes

2020 ◽  
Author(s):  
Bincheng Tang ◽  
Jia min Qiu ◽  
Shen qiang HU ◽  
Liang Li ◽  
Ji wen Wang
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Er Stress ◽  
Mrna Expression ◽  
Coenzyme A ◽  
Acid Tolerance ◽  
Mrna Levels ◽  
Primary Hepatocytes

Abstract BackgroundUnlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid tolerance of goose primary hepatocytes.MethodsTo evaluate the palmitic acid tolerance of cultured hepatocytes, MTT was examined to reflect the effect of palmitic acid on cell viability, and quantitative PCR was used to detect the mRNA expression levels of several genes related to ER stress, inflammation, and apoptosis, and the role of SCD1 in palmitic acid tolerance of goose hepatocytes was explored using RNA interfere.ResultsOur results indicated that goose hepatocytes exhibited a higher tolerant capacity to palmitic acid than human hepatic cell line (LO2 cells). Furthermore, the mRNA levels of fatty acid desaturation-related genes (SCD1 and FADS2) and fatty acid elongate enzyme-related gene (ELOVL6) were significantly upregulated in goose primary hepatocytes treated with 0.6 mM palmitic acid. However, in cultured LO2 cells, expression of ER stress-related genes (XBP, BIP and ATF6), inflammatory response-related genes (IL-6, IL-1β and IFN-γ) and apoptosis-related genes (Bax, Bcl-2, Caspase-3 and Caspase-9) was significantly enhanced by the addition of 0.6 mM palmitic acid. Additionally, siRNA-mediated downregulation of SCD1 significantly reduced the palmitic acid tolerance of goose primary hepatocytes under the treatment of 0.6 mM palmitic acid; meanwhile, the mRNA expression of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the PI3K/AKT, FoxO1, mTOR and AMPK pathways (AKT1, AKT2, FOXO1 and SIRT1), as well as the protein expression of cytochrome C and the apoptosis rate were also upregulated.ConclusionIn conclusion, our data suggested that SCD1 is involved in enhancing the palmitic acid tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.

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