scholarly journals Adrenaline Stimulation of Phospholipid Metabolism in Adipocyte Ghosts

1987 ◽  
Vol 40 (4) ◽  
pp. 405
Author(s):  
David Mann ◽  
Audrey M Bersten
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Adenylate Cyclase ◽  
Phospholipid Metabolism ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Membrane Phospholipids ◽  
Dose Dependent ◽  
Stimulation Of

The incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1_14 C] stearic, [1_14 C] linoleic or [l_14C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10-5 M adrenaline and 10-7 M adenosine. The a-agonist phenylephrine and the ~-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.

Physiological concentrations of insulin and T3 stimulate 3T3-L1 adipocyte acyl-CoA synthetase gene transcription

1996 ◽  
Vol 270 (5) ◽  
pp. E873-E881 ◽  
Author(s):  
M. S. Kansara ◽  
A. K. Mehra ◽  
J. Von Hagen ◽  
E. Kabotyansky ◽  
P. J. Smith
Keyword(s):  
Gene Transcription ◽  
Fold Increase ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Reciprocal Regulation ◽  
Stearoyl Coa Desaturase ◽  
Dose Dependent ◽  
Long Chain ◽  
Stimulation Of

Acyl-CoAsynthetase (ACS) is a key gene for cellular utilization of long-chain fatty acids. We characterized its regulation by physiological concentrations of insulin that acutely regulate metabolism. Our results demonstrate that subnanomolar insulin rapidly and maximally stimulates ACS gene transcription in the absence of protein synthesis; 0.5 nM insulin produced a 2.3 +/- 0.1-fold increase in ACS mRNA levels and induced ACS gene transcription 2.4 +/- 0.3-fold. The insulin sensitivity of ACS was compared with lipoprotein lipase (LPL) and stearoyl-CoA desaturase-1 (SCD-1), which were both less sensitive to insulin. Physiological triiodothyronine (10 nm) also induced ACS mRNA 2.4 +/- 0.1-fold and gene transcription 2.8 +/- 0.3-fold and coordinately induced LPL and SCD-1 mRNA and gene transcription. Because insulin and adenosine 3',5'-cyclic monophosphate often regulate genes involved in lipid and carbohydrate metabolism in a reciprocal manner, we evaluated effects of 1-methyl-3-isobutylxanthine (MIX).ACS mRNA levels were strongly downregulated by MIX in a dose-dependent manner, and ACS gene transcription inhibited in a coordinate manner with LPL and SCD-1. These data demonstrate a uniquely sensitive pattern of stimulation of ACS gene transcription by insulin with reciprocal regulation by MIX, and they suggest a significant role for ACS as a tightly regulated “gatekeeper” gene participating in the control of adipocyte metabolism.

scholarly journals Mechanisms involved in intracellular calcium mobilization in isolated rat islets of Langerhans

1987 ◽  
Vol 244 (3) ◽  
pp. 669-674 ◽  
Author(s):  
N G Morgan ◽  
G M Rumford ◽  
W Montague
Keyword(s):  
Arachidonic Acid ◽  
Islets Of Langerhans ◽  
Inositol Trisphosphate ◽  
Arachidonic Acid Content ◽  
Dependent Manner ◽  
Amphipathic Peptide ◽  
Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Dose Dependent ◽  
Stimulation Of

1. The rate of 45Ca2+ efflux from prelabelled rat islets of Langerhans was stimulated by carbachol in a dose-dependent manner. 2. Significant stimulation occurred in the presence of 0.2 microM-carbachol; the response was half-maximal at 3-5 microM and was maximal at 20 microM. 3. Stimulation of 45Ca2+ efflux by carbachol was not dependent on the presence of extracellular Ca2+ and was enhanced in Ca2+-depleted medium. 4. Stimulation of 45Ca2+ efflux by 5 microM-carbachol occurred independently of any change in [3H]arachidonic acid release in prelabelled islets, and probably reflected generation of inositol trisphosphate in the cells. 5. The amphipathic peptide melittin failed to increase islet-cell 45Ca2+ efflux at a concentration of 1 microgram/ml, and caused only a modest increase at 10 micrograms/ml. 6. Despite its failure to increase 45Ca2+ efflux, melittin at 1 microgram/ml caused a marked enhancement of 3H release from islets that had been prelabelled with [3H]arachidonic acid. 7. The stimulation of 3H efflux caused by melittin correlated with a dose-dependent increase in the unesterified [3H]arachidonic acid content of prelabelled islets and with a corresponding decrease in the extent of labelling of islet phospholipids. 8. Combined addition of melittin (1 microgram/ml) and 5 microM-carbachol to perifused islets failed to augment 45Ca2+ efflux relative to that elicited by carbachol alone. 9. The data indicate that melittin promotes an increase in arachidonic acid availability in intact rat islets. They do not, however, support the proposal that this can either directly reproduce or subsequently modify the extent of intracellular Ca2+ mobilization induced by agents that cause an increase in inositol trisphosphate.

scholarly journals Biosynthesis of platelet-activating factor (PAF) in human polymorphonuclear leucocytes. The role of lyso-PAF disposal and free arachidonic acid

1990 ◽  
Vol 268 (1) ◽  
pp. 91-98 ◽  
Author(s):  
M D C Garcia ◽  
S Fernandez-Gallardo ◽  
M A Gijon ◽  
C Garcia ◽  
M L Nieto ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Platelet Activating Factor ◽  
Inhibitory Effect ◽  
Eicosatetraenoic Acid ◽  
Polymorphonuclear Leucocytes ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Dose Dependent

Theophylline and 1-methyl-3-isobutylxanthine (MIX), compounds that block eicosanoid formation and modulate phospholipase A2 activity, inhibited in a dose-dependent manner the formation of both leukotriene B4 (LTB4) and platelet-activating factor (PAF) by human polymorphonuclear leucocytes (PMN) in response to ionophore A23187. Theophylline and MIX lacked any inhibitory effect on acetyl-CoA: lyso-PAF acetyltransferase activity, which is the rate-limiting step for PAF biosynthesis in PMN. The effect of theophylline and MIX on PAF formation could be reversed by incubating the cells in the presence of 1-10 microM exogenous lyso-PAF. Incubation of PMN homogenates in the presence of unsaturated non-esterified fatty acids resulted in dose-dependent inhibition of the acetyltransferase. This effect was linked to the presence of a free carboxyl group, since both arachidonic acid methyl ester and palmitoyl-arachidonoyl phosphatidylcholine lacked inhibitory activity. This inhibitory effect was also dependent on the number of double bonds, since arachidonic acid (C20:4) and eicosapentaenoic acid (C20:5) displayed maximal effect. Kinetic analysis showed that the effect of arachidonic acid was consistent with competitive inhibition, with a Ki value of about 19 microM. Oxidative metabolites of arachidonic acid showed a lesser inhibitory effect with the following order of potency: arachidonic acid greater than 15-HETE (15-hydroxy-6,8,11,14-eicosatetraenoic acid) greater than LTB4 greater than 5-HETE (5-hydroxy-6,8,11,14-eicosatetraenoic acid) greater than lipoxin A4. Examination of enzymes involved in CoA-dependent acylation revealed a low activity of both arachidonoyl-CoA synthetase and arachidonoyl-CoA: lyso-PAF arachidonoyltransferase. These data indicate a strong influence on PAF biosynthesis of the products of the phospholipase A2 reaction, with lyso-PAF disposal being a critical event for PAF formation, and unsaturated fatty acids acting as feed-back inhibitors. The conversion of arachidonic acid via oxidative metabolism into less active inhibitors of acetyl-CoA:lyso-PAF acetyltransferase seems to be an additional mechanism of modulation of this enzyme activity, linked to the function of lipoxygenases. Finally, the enzyme activities involved in arachidonoyl-CoA-dependent acylation of lyso-PAF show a low efficiency in capturing arachidonic acid.

scholarly journals Influence of arachidonic acid on indices of phospholipase A2 activity in the human neutrophil

1993 ◽  
Vol 291 (3) ◽  
pp. 825-831 ◽  
Author(s):  
J D Winkler ◽  
C M Sung ◽  
W C Hubbard ◽  
F H Chilton
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Protein Kinase ◽  
Phospholipase A2 ◽  
Human Neutrophils ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Pla2 Activity ◽  
Tetraenoic Acid ◽  
Stimulation Of

The present studies were conducted to understand better the regulation of phospholipase A2 (PLA2)-dependent mobilization of lipid mediators by arachidonic acid (C20:4). After stimulation of human neutrophils, g.l.c./m.s. analysis of non-esterified fatty acids indicated that the quantity of C20:4 increased as a function of time after stimulation, from undetectable quantities to > 800 pmol/10(7) cells. In contrast with C20:4, the quantities of other free fatty acids such as oleic and linoleic were high in resting cells and did not change after stimulation. Some 15% of the C20:4 released from cellular lipids remained cell-associated. To examine the effect of C20:4 on its own release, neutrophils were exposed to [2H8]C20:4, to differentiate it by g.l.c./m.s. from naturally occurring C20:4. In A23187-stimulated neutrophils, low concentrations (5-10 microM) of [2H8]C20:4 added just before A23187 increased the quantity of C20:4 produced by the cell, whereas higher concentrations (30-50 microM) decreased the quantity of C20:4 released from phospholipids. As other measures of PLA2 activity, the effects of C20:4 on production of platelet-activity factor (PAF) and leukotriene B4 (LTB4) were assessed. C20:4 treatment just before stimulation of neutrophils blocked PAF and LTB4 production in a concentration-dependent manner (IC50 10-20 microM). The effect of C20:4 was not blocked by the cyclo-oxygenase inhibitor naproxine (10 microM), nor could it be mimicked by 1 microM LTB4, 5-hydroxyeicosa-6,8,11,14-tetraenoic acid (5HETE), 5-hydroperoxyeicosa-6,8,11,14-tetraenoic acid (5HPETE) or 15-hydroxyeicosa-5,8,11,13-tetraenoic acid (15HETE). The 5-lipoxygenase (5LO) inhibitor zileuton induced a concentration-dependent decrease in PAF, with a maximal effect of a 50% decrease at 10-50 microM. The decrease in PAF by the 5LO inhibitor could not be circumvented by addition of 1 microM 5HETE, 5HPETE and LTB4, and may be attributed to the capacity of zileuton to increase the quantity of C20:4 in A23187-treated neutrophils. The inhibitory effect of C20:4 (20-40 microM) on PAF production could be antagonized by the protein kinase C inhibitor staurosporine (30 nM), but not by inhibitors of protein kinase A, tyrosine kinase or calmodulin kinase II. Taken together, these data demonstrate that C20:4 is selectively released from membrane phospholipids of A23187-stimulated neutrophils, and this C20:4 may play an important role in regulating the mobilization of C20:4 by altering PLA2 activity.

Angiotensin-induced relaxation in isolated dog renal and cerebral arteries

1981 ◽  
Vol 240 (2) ◽  
pp. H247-H254 ◽  
Author(s):  
N. Toda ◽  
M. Miyazaki
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Cerebral Arteries ◽  
Dependent Manner ◽  
Rat Stomach ◽  
Middle Cerebral Arteries ◽  
Dose Dependent ◽  
Relaxing Effect ◽  
Indomethacin Treatment ◽  
Stimulation Of

Helically cut strips of dog renal and cerebral (basilar and middle cerebral) arteries contracted with prostaglandin (PG) F2 alpha relaxed in response to angiotensin II (AII; 10(-9) to 10(-7) M) in a dose-dependent manner. In renal arterial strips, the relaxation was preceded by a transient contraction. Both the relaxation and the contraction induced by AII were suppressed by [Sar1,Ala8]AII or [Sar1,Ile8]AII. Treatment with propranolol, atropine, hexamethonium, cocaine, aminophylline, cimetidine, or ouabain failed to alter the relaxing effect of AII. The peptide-induced relaxation was reversed to a contraction by aspirin or indomethacin. Treatment with tranylcypromine or 15-hydroperoxy arachidonic acid suppressed the relaxation induced by AII in renal and cerebral arteries but did not alter relaxations induced by PGI2 or K+ (5 mM). In experiments with superfused dog renal and coronary arteries and rat stomach strips, the renal arteries in response to AII released a prostaglandin like substance; the release was suppressed by [Sar1,Ala8]AII or indomethacin. It appears that the relaxation of isolated dog renal and cerebral arteries induced by AII is mediated by the release of PGI2, which is associated with stimulation of AII receptors.

Arachidonic acid increases cytosolic calcium and stimulates hormone release in rat lactotrophs

1995 ◽  
Vol 268 (6) ◽  
pp. E1215-E1223 ◽  
Author(s):  
M. M. Roudbaraki ◽  
P. Vacher ◽  
R. Drouhault
Keyword(s):  
Arachidonic Acid ◽  
Cytosolic Calcium ◽  
Pituitary Cells ◽  
Membrane Phospholipids ◽  
Dual Emission ◽  
Surface Receptors ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Dose Dependent ◽  
Stimulation Of

Arachidonic acid (AA) released from membrane phospholipids after activation of surface receptors causes cellular signaling actions in neurons and endocrine cells, including stimulation of prolactin (PRL) release from dissociated rat pituitary cells and clonal cells of the GH3 pituitary tumor line. In the present study, we investigated the effect of exogenous AA on PRL release from dispersed pituitary cells and tried to elucidate the mechanism involved in this process. The effects of AA on cytosolic Ca2+ concentration ([Ca2+]i) were studied using dual-emission microspectrofluorometry in identification lactotrophs and on PRL release in dispersed pituitary cell populations. AA had a dose-dependent effect on [Ca2+]i. At 1 microM, the Ca2+ increase was biphasic: a mobilization of intracellular Ca2+ from intracellular stores was followed by stimulation of Ca2+ influx. For lower concentrations (10 and 100 nM), only the stimulation of Ca2+ influx was observed. AA-induced Ca2+ influx and PRL release were not due to the stimulation of a phorbol 12-myristate 13-acetate-sensitive protein kinase C. In the same way, AA-stimulated PRL release and intracellular Ca2+ increase were independent of intracellular thapsigargin-sensitive Ca2+ pools. Furthermore, blockade of Ca2+ channels suppressed AA-induced PRL release. We hypothesize that Ca2+ influx plays a major role in AA-induced PRL release.

scholarly journals Biofabricated Fatty Acids-Capped Silver Nanoparticles as Potential Antibacterial, Antifungal, Antibiofilm and Anticancer Agents

2021 ◽  
Vol 14 (2) ◽  
pp. 139
Author(s):  
Mohammad Azam Ansari ◽  
Sarah Mousa Maadi Asiri ◽  
Mohammad A. Alzohairy ◽  
Mohammad N. Alomary ◽  
Ahmad Almatroudi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Silver Nanoparticles ◽  
Anticancer Agents ◽  
Sem Analysis ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Anticancer Efficacy ◽  
Hct 116 ◽  
Hct 116 Cells ◽  
Dose Dependent

The current study demonstrates the synthesis of fatty acids (FAs) capped silver nanoparticles (AgNPs) using aqueous poly-herbal drug Liv52 extract (PLE) as a reducing, dispersing and stabilizing agent. The NPs were characterized by various techniques and used to investigate their potent antibacterial, antibiofilm, antifungal and anticancer activities. GC-MS analysis of PLE shows a total of 37 peaks for a variety of bio-actives compounds. Amongst them, n-hexadecanoic acid (21.95%), linoleic acid (20.45%), oleic acid (18.01%) and stearic acid (13.99%) were found predominately and most likely acted as reducing, stabilizing and encapsulation FAs in LIV-AgNPs formation. FTIR analysis of LIV-AgNPs shows some other functional bio-actives like proteins, sugars and alkenes in the soft PLE corona. The zone of inhibition was 10.0 ± 2.2–18.5 ± 1.0 mm, 10.5 ± 2.5–22.5 ± 1.5 mm and 13.7 ± 1.0–16.5 ± 1.2 against P. aeruginosa, S. aureus and C. albicans, respectively. LIV-AgNPs inhibit biofilm formation in a dose-dependent manner i.e., 54.4 ± 3.1%—10.12 ± 2.3% (S. aureus), 72.7 ± 2.2%–23.3 ± 5.2% (P. aeruginosa) and 85.4 ± 3.3%–25.6 ± 2.2% (C. albicans), and SEM analysis of treated planktonic cells and their biofilm biomass validated the fitness of LIV-AgNPs in future nanoantibiotics. In addition, as prepared FAs rich PLE capped AgNPs have also exhibited significant (p < 0.05 *) antiproliferative activity against cultured HCT-116 cells. Overall, this is a very first demonstration on employment of FAs rich PLE for the synthesis of highly dispersible, stable and uniform sized AgNPs and their antibacterial, antifungal, antibiofilm and anticancer efficacy.

Fatty acids and cytokine mRNA expression in human osteoblastic cells: a specific effect of arachidonic acid

2002 ◽  
Vol 102 (4) ◽  
pp. 403-409 ◽  
Author(s):  
G. PRIANTE ◽  
L. BORDIN ◽  
E. MUSACCHIO ◽  
G. CLARI ◽  
B. BAGGIO
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Mrna Expression ◽  
Specific Effect ◽  
Significant Inhibition ◽  
Cytokine Gene Expression ◽  
Dependent Manner ◽  
Human Osteoblast ◽  
Cytokine Mrna ◽  
Cytokine Mrna Expression

Epidemiological, clinical and experimental evidence suggests that fatty acids have a modulatory effect on bone metabolism in animals and humans. To investigate this hypothesis, we evaluated the effects of three different fatty acids, arachidonic acid (AA), eicosapentaenoic acid (EPA) and oleic acid (OA), on the expression of cytokines involved in bone remodelling. Cytokine mRNAs in the human osteoblast-like cell line MG-63 were quantified by reverse transcription-PCR. AA induced increased expression of interleukin-1α, interleukin-1β, tumour necrosis factor-α and macrophage colony-stimulating factor mRNAs in a time- and dose-dependent manner. EPA and OA had no stimulatory effects, but instead caused a significant inhibition of AA-induced cytokine mRNA expression. Cell treatment with calphostin C, an inhibitor of protein kinase C (PKC), and cellular PKC down-regulation experiments independently resulted in significant inhibition of AA-induced cytokine expression, suggesting that a PKC-dependent mechanism accounts for the effects of AA on cytokine production. In conclusion, our study demonstrates specific effects of fatty acids on cytokine gene expression in human osteoblast-like cells. The clinical relevance of our findings requires further investigation.

scholarly journals Effect of different long-chain fatty acids on cholecystokinin releasein vitroand energy intake in free-living healthy males

2012 ◽  
Vol 108 (4) ◽  
pp. 755-758 ◽  
Author(s):  
Charlotte J. Harden ◽  
Adam N. Jones ◽  
Tannia Maya-Jimenez ◽  
Margo E. Barker ◽  
Natalie J. Hepburn ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Chain Length ◽  
Energy Intake ◽  
Acyl Chain ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Long Chain ◽  
Healthy Males ◽  
Cck Release ◽  
Chain Fatty Acids

Long-chain fatty acids have been shown to suppress appetite and reduce energy intake (EI) by stimulating the release of gastrointestinal hormones such as cholecystokinin (CCK). The effect of NEFA acyl chain length on these parameters is not comprehensively understood. Anin vitroscreen tested the capacity of individual NEFA (C12 to C22) to trigger CCK release. There was a gradient in CCK release with increasing chain length. DHA (C22) stimulated significantly (P < 0·01) more CCK release than all other NEFA tested. Subsequently, we conducted a randomised, controlled, crossover intervention study using healthy males (n18). The effects of no treatment (NT) and oral doses of emulsified DHA-rich (DHA) and oleic acid (OA)-rich oils were compared using 24 h EI as the primary endpoint. Participants reported significantly (P = 0·039) lower total daily EI (29 % reduction) with DHA compared to NT. There were no differences between DHA compared to OA and OA compared to NT. There was no between-treatment difference in the time to, or EI of, the first post-intervention eating occasion. It is concluded that NEFA stimulate CCK release in a chain length-dependent manner up to C22. These effects may be extended to thein vivosetting, as a DHA-based emulsion significantly reduced short-term EI.

scholarly journals Dietary fat and the diabetic state alter insulin binding and the fatty acyl composition of the adipocyte plasma membrane

1988 ◽  
Vol 253 (2) ◽  
pp. 417-424 ◽  
Author(s):  
C J Field ◽  
E A Ryan ◽  
A B Thomson ◽  
M T Clandinin
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Plasma Membrane ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Insulin Binding ◽  
Fatty Acyl ◽  
Membrane Composition ◽  
Membrane Phospholipids ◽  
Diabetic State

Control and diabetic rats were fed on semi-purified high-fat diets providing a polyunsaturated/saturated fatty acid ratio (P/S) of 1.0 or 0.25, to examine the effect of diet on the fatty acid composition of major phospholipids of the adipocyte plasma membrane. Feeding the high-P/S diet (P/S = 1.0) compared with the low-P/S diet (P/S = 0.25) increased the content of polyunsaturated fatty acids in membrane phospholipids in both control and diabetic animals. The diabetic state decreased the content of polyunsaturated fatty acids, particularly arachidonic acid, in adipocyte membrane phospholipids. The decrease in arachidonic acid in membrane phospholipids of diabetic animals tended to be normalized to within the control values when high-P/S diets were given. For control animals, altered plasma-membrane composition was associated with change in insulin binding, suggesting that change in plasma-membrane composition may have physiological consequences for insulin-stimulated functions in the adipocyte.

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