Eicosapentaenoic and dihomo gamma linolenic acid metabolism by cultured rat mesangial cells

1989 ◽  
Vol 256 (1) ◽  
pp. C101-C108 ◽  
Author(s):  
L. A. Scharschmidt ◽  
N. B. Gibbons ◽  
R. Neuwirth
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Acid Metabolism ◽  
Mesangial Cells ◽  
Gamma Linolenic Acid ◽  
Significant Extent ◽  
Glomerular Function ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Stimulation Of

To better understand the effects of dietary fatty acid manipulations on glomerular function, we compared mesangial incorporation, release, and metabolism of arachidonic (AA), eicosapentaenoic (EPA), and dihomo gamma linolenic (DHG) acids. We found marked differences in mesangial handling of these fatty acids. AA was incorporated into lipids of mesangial cells much more rapidly than EPA or DHG. Ionophore-induced stimulation of fatty acid release from mesangial cells prelabeled with [14C]AA, [14C]EPA, or [14C]DHG caused a release of labeled AA greater than DHG much less than EPA, respectively. Preloading mesangial cells with DHG or EPA for 24 h reduced subsequent basal, ionophore-, and hormone-stimulated prostaglandin E2 (PGE2) synthesis. Finally, unlike AA, neither EPA nor DHG was converted to a significant extent by mesangial cyclooxygenase or lipoxygenase. Thus the mesangial metabolism of DHG and EPA differs both quantitatively and qualitatively from that of AA. Furthermore, EPA and DHG inhibit metabolism of AA at the level of mesangial cyclooxygenase.

scholarly journals Biochemical actions of vasoactive peptide hormones. Time-synchronized activation of lipolysis and decreased fatty-acid release by bradykinin and angiotensin in the perfused rabbit kidney

1980 ◽  
Vol 192 (1) ◽  
pp. 127-131 ◽  
Author(s):  
M Schwartzman ◽  
A Raz
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Time Lag ◽  
Rabbit Kidney ◽  
Subsequent Decrease ◽  
Fatty Acid Release ◽  
Initial Activation ◽  
Acid Release ◽  
Sequential Processes ◽  
Vasoactive Peptide

Bradykinin and angiotensin administered to the isolated perfused rabbit kidney activate two sequential processes: (1) a selective release of the prostaglandin precursor arachidonate with concomitant partial conversion of the arachidonate into prostaglandin E2; (2) activation of a process that leads to decreased release of all fatty acids in the perfusate. There is a time lag of approx. 1 min between the initial activation of the arachidonate-specific deacylation reaction that is coupled to prostaglandin generation, and the subsequent decrease in the release of all fatty acids. This synchronized cycle provides for instant generation of required amounts of prostaglandins and at the same time serves to conserve cellular arachidonate.

Epinephrine-insulin antagonism on free fatty acid release

1961 ◽  
Vol 201 (5) ◽  
pp. 815-818 ◽  
Author(s):  
John J. Spitzer ◽  
William T. McElroy
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Blood Sugar ◽  
Drug Administration ◽  
Hepatic Uptake ◽  
Fatty Acid Release ◽  
Plasma Ffa ◽  
Acid Release

The effects of epinephrine or norepinephrine were studied in dogs receiving insulin plus glucose prior to and during administration of the amine. Epinephrine caused a significantly smaller elevation of free fatty acids (FFA) with than without insulin plus glucose administration. Blood sugar responses were quantitatively similar. Epinephrine increased both hepatic uptake of FFA and hepatic release of glucose; these changes were similar to the ones found previously in dogs not receiving insulin plus glucose. The action of norepinephrine on elevating plasma FFA was only slightly and not significantly affected by the administration of insulin plus glucose. When the order of drug administration was reversed, infusion of insulin plus glucose lowered plasma FFA levels and hepatic FFA uptake in animals already receiving either epinephrine or nonepinephrine.

Fatty acid metabolism and cell proliferation: IV. Effect of prostanoid biosynthesis from endogenous fatty acid release with cyclosporin-A

Lipids ◽  
1983 ◽  
Vol 18 (8) ◽  
pp. 566-569 ◽  
Author(s):  
Jenifer A. Lindsey ◽  
Nobuhiro Morisaki ◽  
Judith M. Stitts ◽  
Richard A. Zager ◽  
David G. Cornwell
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
Cyclosporin A ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Endogenous Fatty Acid ◽  
Fatty Acid Release ◽  
Acid Release

Stimulation of Phosphorylcholine–Glyceride Transferase Activity by Unsaturated Fatty Acids

1973 ◽  
Vol 51 (11) ◽  
pp. 1479-1486 ◽  
Author(s):  
Michael Sribney ◽  
Eileen M. Lyman
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Unsaturated Fatty Acids ◽  
Small Extent ◽  
Fatty Acid Esters ◽  
Transferase Activity ◽  
Significant Extent ◽  
Acyltransferase Activity ◽  
Acid Esters ◽  
Stimulation Of

A number of unsaturated fatty acids markedly stimulate chicken liver microsomal phosphorylcholine–glyceride transferase (CDP-choline:1,2-diglyceride cholinephosphotransferase, EC 2.7.8.2). Oleate (0.8 mM) activates this enzyme severalfold only if a mixed diglyceride such as 1-palmitoyl-2-oleoyl-sn-glycerol is used as a substrate for the reaction. Dipalmitin and diolein incorporation into lecithin is not stimulated to any significant extent by unsaturated fatty acids. Fatty acid esters and numerous detergents either inhibit the enzyme or have no effect. Phosphorylethanolamine–glyceride transferase (CDP-ethanolamine:1,2-diglyceride ethanolaminephosphotransferase, EC 2.7.8.1) activity is only very slightly stimulated while diglyceride O-acyltransferase activity is inhibited to a small extent.

Action of phospholipases A2 and C on free fatty acid release during complete ischemia in rat neocortex

1992 ◽  
Vol 76 (4) ◽  
pp. 648-651 ◽  
Author(s):  
Atsushi Umemura ◽  
Hideo Mabe ◽  
Hajime Nagai ◽  
Fumihiko sugino
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Phospholipase C ◽  
Phenylmethylsulfonyl Fluoride ◽  
Content Type ◽  
Rat Neocortex ◽  
Fatty Acid Release ◽  
Acid Release

✓ The levels of brain free fatty acids rapidly increase after the onset of ischemia. The purpose of this study was to investigate the action of phospholipases A2 and C during complete ischemia based on the effects of a phospholipase C inhibitor (phenylmethylsulfonyl fluoride) and the N-methyl-D-aspartate antagonist MK-801 on the release of free fatty acids in rat neocortex. Complete brain ischemia was induced in rats with cardiac arrest by intracardiac injection of KC1. Free fatty acid levels in the neocortex were measured 0, 2, 4, and 8 minutes after cardiac arrest. Phenylmethylsulfonyl fluoride inhibited the release of free fatty acids primarily from phosphatidylinositol during the first 2 minutes of ischemia and from phosphatidylcholine and phosphatidylethanolamine at 4 to 8 minutes of ischemia. Conversely, MK-801 inhibited free fatty acid release mainly from phosphatidylcholine and phosphatidylethanolamine at 2 to 4 minutes of ischemia. These results indicate that the release of free fatty acids during the first 2 minutes of ischemia can be attributed mostly to the action of phospholipase C, and that the activation of phospholipase C further influences the activation of phospholipase A2 in the subsequent course, while phospholipase A2 predominantly acts after 2 minutes of ischemia.

scholarly journals The response of adipocyte glucose metabolism and fatty acid release to adenosine deaminase, insulin and perifusion. Investigation of intermediary metabolism by perifusion

1988 ◽  
Vol 251 (3) ◽  
pp. 733-737
Author(s):  
R D Harper
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Adenosine Deaminase ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Intermediary Metabolism ◽  
Glucose Incorporation ◽  
Fatty Acid Release ◽  
Acid Release

Adipocytes incubated with adenosine deaminase (ADA) showed: (1) increased amounts of fatty acids in the medium; (2) increased glucose incorporation into acylglycerol glycerol; (3) decreased glucose incorporation into acylglycerol fatty acids; (4) a co-ordinate decrease in the sensitivity of lipolysis and glucose incorporation into acylglycerol to insulin; (5) similar effects on glucose incorporations in perifused and normal incubations. The decrease in fatty acid synthesis by perfusion was found to be dependent on the presence of insulin or fatty acids, and independent of the effects of ADA. The significance of the effects of perifusion, ADA and insulin are discussed in relation to effects of fatty acids.

scholarly journals Free fatty acid release from vegetable and bovine milk fat-based infant formulas and human milk during two-phase in vitro digestion

2019 ◽  
Vol 10 (4) ◽  
pp. 2102-2113 ◽  
Author(s):  
Jeske H. J. Hageman ◽  
Jaap Keijer ◽  
Trine Kastrup Dalsgaard ◽  
Lara W. Zeper ◽  
Frédéric Carrière ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Milk Fat ◽  
Bovine Milk ◽  
In Vitro Digestion ◽  
Infant Formulas ◽  
Two Phase ◽  
Fatty Acid Release ◽  
Acid Release

The profile of fatty acids released during in vitro digestion of vegetable and bovine milk fat-based infant formula differ.

scholarly journals Glycerol and fatty acid kinetics in rainbow trout: effects of endurance swimming

1999 ◽  
Vol 202 (3) ◽  
pp. 279-288 ◽  
Author(s):  
S.F. Bernard ◽  
S.P. Reidy ◽  
G. Zwingelstein ◽  
J. Weber
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Rainbow Trout ◽  
Body Temperature ◽  
Submaximal Exercise ◽  
Membrane Phospholipids ◽  
Esterified Fatty Acids ◽  
Fatty Acid Release ◽  
Acid Release

Continuous infusions of 2-[3H]glycerol and 1-[14C]palmitate were performed in vivo in rainbow trout to measure the effects of prolonged swimming on (1) the rate of appearance of glycerol (Ra glycerol or lipolytic rate), (2) the rate of appearance of non-esterified fatty acids (Ra NEFA) and (3) the rate of triacylglycerol:fatty acid cycling (TAG:FA cycling or re-esterification). Our goals were to test the hypothesis that sustained exercise for up to 4 days causes the progressive mobilization of triacylglycerol reserves to supply fuel to contracting muscles, and to assess whether TAG:FA cycling plays a role in the regulation of NEFA availability in teleosts. Contrary to expectation, the rates of lipolysis and fatty acid release in resting trout are not affected by endurance exercise. Unlike mammals, which increase the rate of lipolysis by two- to fourfold during submaximal exercise, these active teleosts do not mobilize triacylglycerol reserves beyond resting levels to supply more NEFAs to working muscles. Furthermore, they maintain Ra glycerol and Ra NEFA well in excess of oxidative fuel requirements even at rest. More than two-thirds of the NEFAs produced are re-esterified, but the results show that TAG:FA cycling is not involved in the regulation of NEFA availability during or after swimming. We propose that the observed high rates of re-esterification represent an important feature of ectothermic metabolism that allows the restructuring of membrane phospholipids to be synchronized with frequent changes in body temperature.

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