scholarly journals Vascular Consequences of Metabolic Syndrome Related Shifts in Cyclooxygenase Mediated Arachidonic Acid Metabolism

2011 ◽  
Author(s):  
Adam G. Goodwill
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism

scholarly journals 17βEstradiol Modulates Perfusion Pressure and Expression of 5-LOX and CYP450 4A in the Isolated Kidney of Metabolic Syndrome Female Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
A. M. Zúñiga-Muñoz ◽  
V. Guarner Lans ◽  
E. Soria-Castro ◽  
E. Diaz-Diaz ◽  
R. Torrico-Lavayen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Cytochrome P450 ◽  
Acid Metabolism ◽  
Perfusion Pressure ◽  
Arachidonic Acid Metabolism ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Female Wistar Rats ◽  
Cytochrome P450 4A

Prevalence of metabolic syndrome and progression of nephropathy depend on sex. We examined a protective effect of estradiol against nephropathy in metabolic syndrome through the modulation of the arachidonic acid metabolism by activating the 5-lipoxygenase and cytochrome p450 4A pathways. 28 female Wistar rats were divided into four groups of seven animals each: control, intact metabolic syndrome, ovariectomized metabolic syndrome, and metabolic syndrome ovariectomized plus estradiol. Blood pressure, body weight, body fat, triglycerides, insulin, HOMA-index, albuminuria, and TNF-αwere increased in ovariectomized metabolic syndrome rats (p<0.001). The perfusion pressure in isolated kidneys of ovariectomized metabolic syndrome rats in presence of 4 μg of arachidonic acid was increased. The inhibitors of the arachidonic acid metabolism Baicalein, Miconazole, and Indomethacin in these rats decreased the perfusion pressure by 57.62%, 99.83%, and 108.5%, respectively and they decreased creatinine clearance and the arachidonic acid percentage. Phospholipase A2expression in the kidney of ovariectomized metabolic syndrome rats was not modified. 5-lipoxygenase was increased in metabolic syndrome ovariectomized rats while cytochrome p450 4A was decreased. In conclusion, the loss of estradiol increases renal damage while the treatment with estradiol benefits renal function by modulating arachidonic acid metabolism through the 5-lipoxygenase and cytochrome p450 4A pathways.

Altered arachidonic acid metabolism impairs functional vasodilation in metabolic syndrome

2006 ◽  
Vol 290 (1) ◽  
pp. R134-R138 ◽  
Author(s):  
Lusha Xiang ◽  
Jay S. Naik ◽  
Benjamin L. Hodnett ◽  
Robert L. Hester
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Sodium Nitroprusside ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Zucker Rats ◽  
Thromboxane Receptor ◽  
Obese Zucker Rats ◽  
Prostacyclin Analog ◽  
Arteriolar Diameter

These studies tested the hypothesis that in obese Zucker rats (OZRs), a model of metabolic syndrome, the impaired functional vasodilation is due to increased thromboxane receptor (TP)-mediated vasoconstriction and/or decreased prostacyclin-induced vasodilation. Spinotrapezius arcade arterioles from 12-wk-old lean (LZR) and OZR were chosen for microcirculatory observation. Arteriolar diameter (5 LZR and 6 OZR) was measured after 2 min of muscle stimulation in the absence or presence of 1 μM SQ-29548 (TP antagonist). Additionally, arteriolar diameter (6 for each group) was measured after application of iloprost (prostacyclin analog; 0.28, 2.8, and 28 μM), arachidonic acid (10 μM), and sodium nitroprusside (0.1, 1, and 10 μM) in the absence or presence of 1 μM SQ-29548. A 10 μM concentration of adenosine was used to induce a maximal dilation. Basal diameters were not different between LZRs and OZRs. Functional hyperemia and arachidonic acid-mediated vasodilations were significantly attenuated in OZR compared with LZR, and treatment with 1 μM SQ-29548 significantly enhanced the dilations in OZRs, although it had no effect in LZRs. Vasodilatory responses to iloprost and sodium nitroprusside (1 and 10 μM) were significantly reduced in OZR. Adenosine-mediated vasodilation was not different between groups. These results suggest that the impaired functional dilation in the OZR is due to an increased TP-mediated vasoconstriction and a decreased PGI2-induced vasodilation.

Regulation of arachidonic acid metabolism in human amnion

1985 ◽  
Vol 110 (1_Suppla) ◽  
pp. S53-S54
Author(s):  
ST. NIESERT ◽  
M. D. MITCHELL ◽  
M. L. CASEY ◽  
P. C. MACDONALD
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Human Amnion

Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

Diabetes ◽  
1988 ◽  
Vol 37 (7) ◽  
pp. 992-996 ◽  
Author(s):  
J. Turk ◽  
J. H. Hughes ◽  
R. A. Easom ◽  
B. A. Wolf ◽  
D. W. Scharp ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Human Pancreatic Islets

The interaction Between Arachidonic Acid Metabolism and Homocysteine

2020 ◽  
Vol 20 ◽  
Author(s):  
Elisa Domi ◽  
Malvina Hoxha ◽  
Bianka Hoxha ◽  
Bruno Zappacosta
Keyword(s):  
Cardiovascular Disease ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Neurological Diseases ◽  
Arachidonic Acid Metabolism ◽  
Epoxyeicosatrienoic Acids ◽  
Pathological Conditions ◽  
Literature Searches ◽  
Hydroxyeicosatetraenoic Acids ◽  
Improve Health

Purpose: Hyperhomocysteinemia (HHcy) has been considered a risk factor for different diseases including cardiovascular disease (CVD), inflammation, neurological diseases, cancer and many other pathological conditions. Likewise, arachidonic acid (AA) metabolism is implicated in both vascular homeostasis and inflammation as shown by the development of CVD following the imbalance of its metabolites. Aim of The Review: This review summarizes how homocysteine (Hcy) can influence the metabolism of AA. Methods: In silico literature searches were performed on PubMed and Scopus as main sources. Results: Several studies have shown that altered levels of Hcy, through AA release and metabolism, can influence the synthesis and the activity of prostaglandins (PGs), prostacyclin (PGI₂), thromboxane (TXA), epoxyeicosatrienoic acids (EETs) and hydroxyeicosatetraenoic acids (HETEs). Conclusions: We believe that by targeting Hcy in AA pathways, novel compounds with better pharmacological and pharmacodynamics benefits may be obtained and that this information is valuable for dietician to manipulate diets to improve health.

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