Induction of Ca-independent PLA2 and conservation of plasmalogen polyunsaturated fatty acids in diabetic heart

2000 ◽  
Vol 279 (1) ◽  
pp. E25-E32 ◽  
Author(s):  
Jane McHowat ◽  
Michael H. Creer ◽  
Kristine K. Hicks ◽  
Janet H. Jones ◽  
Raetreal McCrory ◽  
...  

Diabetes-induced changes in phospholipase A2(PLA2) activity have been measured in several tissues but are undefined in diabetic myocardium. We measured ventricular PLA2 activity in control, streptozotocin-induced diabetic, and insulin-treated diabetic rats and characterized myocardial phospholipids to determine whether diabetes altered myocardial phospholipid metabolism. Increased membrane-associated Ca2+-independent PLA2 (iPLA2) activity was observed in diabetes that was selective for arachidonylated phospholipids. Increased iPLA2 activity was accompanied by an increase in choline lysophospholipids. Diabetes was associated with marked alterations in the phospholipid composition of the myocardium, characterized by decreases in esterified arachidonic and docosahexaenoic acids and increases in linoleic acid. The decrease in polyunsaturated fatty acids was confined to diacylphospholipids, whereas the relative amount of these fatty acids in plasmalogens was increased. Diabetes-induced changes in PLA2 activity, lysophospholipid production, and alterations in phospholipid composition were all reversed by insulin treatment of diabetic animals. Diabetes-induced changes in membrane phospholipid content and phospholipid hydrolysis may contribute to some of the alterations in myocardial function that are observed in diabetic patients.

Lipids ◽  
2008 ◽  
Vol 43 (6) ◽  
pp. 485-497 ◽  
Author(s):  
Sid Ahmed Merzouk ◽  
Meriem Saker ◽  
Karima Briksi Reguig ◽  
Nassima Soulimane ◽  
Hafida Merzouk ◽  
...  

2018 ◽  
Vol 25 (4) ◽  
pp. 363-368
Author(s):  
Victoria Serhiyenko ◽  
Ludmila Serhiyenko ◽  
Alexandr Serhiyenko

Abstract Background and Aims: Diabetic cardiac autonomic neuropathy (DCAN) in type 2 diabetes (T2D) is among the strongest and independent risk markers for future global and cardiac mortality. Material and Methods: Thirty-six patients suffering from T2D and confirmed DCAN were enrolled in this investigation. Depending on the prescribed therapy, patients were allocated into two groups: group 1 was comprised of 15 patients to whom standard hypoglycemic treatment was prescribed (control group), the second received standard hypoglycemic treatment and omega-3 polyunsaturated fatty acids (ω-3 PUFAs, n = 21). The duration of the study was three month. Results: In subjects with T2D and DСAN prescription of ω-3 PUFAs was associated with a significant decrease of aorta augmentation index (AIxao), pulse wave velocity (PWV) during the active period of the day and decrease of AIxao, brachial augmentation index and PWV during the passive period of the day compared with the control group. Therefore, three month of ω-3 PUFAs supplementation to patients with confirmed DCAN and T2D promotes to improvement of arterial stiffness indices. Conclusions: In patients with T2D and СAN treatment with ω-3 PUFAs improved arterial stiffness parameters. The effectiveness of ω-3 PUFAs is not connected with optimization of glycemic control, but is rather the result of a direct drug action on the studied parameters.


1983 ◽  
Vol 50 (04) ◽  
pp. 762-767 ◽  
Author(s):  
Jan H Brox ◽  
Arne Nordøy

SummaryPrimary cultures of human endothelial cell monolayers were incubated with albumin-bound fatty acids of the ω-3 and ω-6 families for a maximum of 24 hrs, to investigate the production of 6-keto-PGF1α, TXB2 and platelet inhibitory activity (PIA). Arachidonic acid was a potent stimulator of all parameters. The release of 6-keto-PGF1α was significantly reduced by equimolar concentrations of linoleic, dihomogamma linolenic and eicosapentaenoic acids, but not by linolenic acid. PIA was not similarity affected.Dihomogamma linolenic add was also a weak stimulator of 6- keto-PGF1α and PIA, but reduced the content of both in the cells after 24 hrs. Eicosapentaenoic and docosahexaenoic acids both depressed 6-keto-PGF1α production but PIA was maintained after 24 hrs. Indomethacin always blocked 6-keto-PGF1α and PIA production. None of the effects correlated to release of 51CR from prelabelled cells.


Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 284 ◽  
Author(s):  
Oxana Kytikova ◽  
Tatyana Novgorodtseva ◽  
Yulia Denisenko ◽  
Marina Antonyuk ◽  
Tatyana Gvozdenko

Asthma is one of the most important medical and social problems of our time due to the prevalence and the complexity of its treatment. Chronic inflammation that is characteristic of asthma is accompanied by bronchial obstruction, which involves various lipid mediators produced from n-6 and n-3 polyunsaturated fatty acids (PUFAs). The review is devoted to modern ideas about the PUFA metabolites—eicosanoids (leukotrienes, prostaglandins, thromboxanes) and specialized pro-resolving lipid mediators (SPMs) maresins, lipoxins, resolvins, protectins. The latest advances in clinical lipidomics for identifying and disclosing the mechanism of synthesis and the biological action of SPMs have been given. The current views on the peculiarities of the inflammatory reaction in asthma and the role of highly specialized metabolites of arachidonic, eicosapentaenoic and docosahexaenoic acids in this process have been described. The possibility of using SPMs as therapeutic agents aimed at controlling the resolution of inflammation in asthma is discussed.


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