Effect of glycine on the cyclooxygenase pathway of the kidney arachidonic acid metabolism in a rat model of metabolic syndrome

2011 ◽  
Vol 89 (12) ◽  
pp. 899-910 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Blanca Ibarra ◽  
Elizabeth Soria-Castro ◽  
Rocío Torrico-Lavayen ◽  
Natalia Pavón ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Rat Model ◽  
Sucrose Solution ◽  
Glycine Receptor ◽  
Renal Perfusion ◽  
Arachidonic Acid Metabolism ◽  
Receptor Expression ◽  
Model Assessment ◽  
Protective Effects

The kidneys are organs that can be severely impaired by metabolic syndrome (MS). This is characterized by the association of various pathologies such as hypertension, dyslipidemia, and type-2 diabetes. Glycine, a nonessential amino acid, is known to possess various protective effects in the kidney, such as a decrease in the deterioration of renal function and a reduction of the damage caused by hypoxia. In a rat model of MS, the effect of glycine on the cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism was studied in isolated perfused kidney. MS was induced in Wistar rats by feeding them a 30% sucrose solution for 16 weeks. The addition of 1% glycine to their drinking water containing 30% sucrose, for 8 weeks, reduced high blood pressure, triglyceride levels, insulin concentration, homeostatis model assessment (HOMA) index, albuminuria, AA concentration in kidney homogenate, renal perfusion pressure, prostaglandin levels, PLA2expression, and COX isoform expression, compared with MS rats that did not receive the glycine supplement. Glycine receptor expression decreased significantly with MS, but glycine treatment increased it. The results suggest that in the MS model, 1% glycine treatment protects the kidney from damage provoked by the high sucrose consumption, by acting as an anti-inflammatory on the COX pathway of AA metabolism in kidney.

scholarly journals Chronic lithium administration attenuates up-regulated brain arachidonic acid metabolism in a rat model of neuroinflammation

2007 ◽  
Vol 102 (3) ◽  
pp. 761-772 ◽  
Author(s):  
Mireille Basselin ◽  
Nelly E. Villacreses ◽  
Ho-Joo Lee ◽  
Jane M. Bell ◽  
Stanley I. Rapoport
Keyword(s):  
Arachidonic Acid ◽  
Rat Model ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism

Effect of gonadectomy on the metabolism of arachidonic acid in isolated kidney of a rat model of metabolic syndrome

Metabolism ◽  
2010 ◽  
Vol 59 (3) ◽  
pp. 414-423 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Mohammed El Hafidi ◽  
Natalia Pavón ◽  
Oscar Infante ◽  
Maria C. Avila-Casado ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Rat Model ◽  
Isolated Kidney

scholarly journals Attenuated PGI2 synthesis in obese Zucker rats

2009 ◽  
Vol 296 (3) ◽  
pp. R715-R721 ◽  
Author(s):  
Benjamin L. Hodnett ◽  
Jennifer A. Dearman ◽  
Cory B. Carter ◽  
Robert L. Hester
Keyword(s):  
Arachidonic Acid ◽  
Muscle Blood Flow ◽  
Arachidonic Acid Metabolism ◽  
Receptor Expression ◽  
Zucker Rats ◽  
Functional Hyperemia ◽  
Tyrosine Residues ◽  
Obese Zucker Rat ◽  
Obese Zucker Rats

In obesity, skeletal muscle blood flow during exercise (functional hyperemia) is impaired. We have indirectly demonstrated that an altered arachidonic acid metabolism is responsible for the impaired functional vasodilation in the obese Zucker rat (OZR), a model of obesity. In this study, we tested the hypothesis that there is an impaired release of PGI2 due to a nitration of PGI2 synthase (PGIS), which is associated with a decreased prostanoid receptor expression. PGI2, PGE2, and thromboxane A2 (TXA2) release were determined in vitro using ELISA under basal conditions and in response to arachidonic acid (AA) administration (50 μM). Immunofluorescence of PGI2 and TXA2 receptors (IP and TP, respectively) was determined in dispersed vascular smooth muscle cells (VSMCs). Nitration of tyrosine residues of the PGIS enzyme was determined using immunoprecipitation and Western blot analysis. Following AA administration, PGI2 and PGE2 release were attenuated in OZR compared with lean Zucker rats (LZR; controls). Basal and AA-induced TXA2 release were not significantly different between groups. IP and TP immunofluorescence were not significantly different between OZR and LZR groups. OZR exhibited elevated nitration of tyrosine residues of PGIS compared with LZR. These results suggest that alterations in the PGI2 pathway (attenuated PGI2 synthesis), and not the TXA2 pathway (normal TXA2 synthesis/no change in TP receptor expression), underlie the attenuated functional hyperemia in the OZR.

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.

scholarly journals Mechanistic Perspectives of Maslinic Acid in Targeting Inflammation

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wei Hsum Yap ◽  
Yang Mooi Lim
Keyword(s):  
Arachidonic Acid ◽  
Inflammatory Diseases ◽  
Experimental Models ◽  
Arachidonic Acid Metabolism ◽  
Protective Effects ◽  
Pentacyclic Triterpene ◽  
Maslinic Acid ◽  
Anti Inflammatory

Chronic inflammation drives the development of various pathological diseases such as rheumatoid arthritis, atherosclerosis, multiple sclerosis, and cancer. The arachidonic acid pathway represents one of the major mechanisms for inflammation. Prostaglandins (PGs) are lipid products generated from arachidonic acid by the action of cyclooxygenase (COX) enzymes and their activity is blocked by nonsteroidal anti-inflammatory drugs (NSAIDS). The use of natural compounds in regulation of COX activity/prostaglandins production is receiving increasing attention. In Mediterranean diet, olive oil and table olives contain significant dietary sources of maslinic acid. Maslinic acid is arising as a safe and novel natural pentacyclic triterpene which has protective effects against chronic inflammatory diseases in variousin vivoandin vitroexperimental models. Understanding the anti-inflammatory mechanism of maslinic acid is crucial for its development as a potential dietary nutraceutical. This review focuses on the mechanistic action of maslinic acid in regulating the inflammation pathways through modulation of the arachidonic acid metabolism including the nuclear factor-kappa B (NF-κB)/COX-2 expression, upstream protein kinase signaling, and phospholipase A2enzyme activity. Further investigations may provide insight into the mechanism of maslinic acid in regulating the molecular targets and their associated pathways in response to specific inflammatory stimuli.

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.

scholarly journals Metformin Affects Cardiac Arachidonic Acid Metabolism and Cardiac Lipid Metabolite Storage in a Prediabetic Rat Model

2021 ◽  
Vol 22 (14) ◽  
pp. 7680
Author(s):  
Denisa Miklankova ◽  
Irena Markova ◽  
Martina Hüttl ◽  
Iveta Zapletalova ◽  
Martin Poruba ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arachidonic Acid ◽  
Fatty Acid ◽  
Rat Model ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Phospholipid Fatty Acid Composition ◽  
Metformin Treatment ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Metformin can reduce cardiovascular risk independent of glycemic control. The mechanisms behind its non-glycemic benefits, which include decreased energy intake, lower blood pressure and improved lipid and fatty acid metabolism, are not fully understood. In our study, metformin treatment reduced myocardial accumulation of neutral lipids—triglycerides, cholesteryl esters and the lipotoxic intermediates—diacylglycerols and lysophosphatidylcholines in a prediabetic rat model (p < 0.001). We observed an association between decreased gene expression and SCD-1 activity (p < 0.05). In addition, metformin markedly improved phospholipid fatty acid composition in the myocardium, represented by decreased SFA profiles and increased n3-PUFA profiles. Known for its cardioprotective and anti-inflammatory properties, metformin also had positive effects on arachidonic acid metabolism and CYP-derived arachidonic acid metabolites. We also found an association between increased gene expression of the cardiac isoform CYP2c with increased 14,15-EET (p < 0.05) and markedly reduced 20-HETE (p < 0.001) in the myocardium. Based on these results, we conclude that metformin treatment reduces the lipogenic enzyme SCD-1 and the accumulation of the lipotoxic intermediates diacylglycerols and lysophosphatidylcholine. Increased CYP2c gene expression and beneficial effects on CYP-derived arachidonic acid metabolites in the myocardium can also be involved in cardioprotective effect of metformin.

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