Abstract
BackgroundLong chain polyunsaturated fatty acids (LCPUFAs) including docosahexaenoic acid and arachidonic acid are suspected to play a key role in the pathogenesis of diabetes. LCPUFAs are known to be preferentially concentrated in specific phospholipids termed as plasmalogens. This study was aimed to highlight potential changes in the metabolism of phospholipids, and particularly plasmalogens, and LCPUFAs at various stages of diabetic retinopathy in humans.Methodology and Principal FindingsWe performed lipidomic analyses on red blood cell membranes from controls and mainly type 2 diabetes mellitus patients with or without retinopathy. The fatty acid composition of erythrocytes was determined by gas chromatography and the phospholipid structure was determined by liquid chromatography equipped with an electrospray ionisation source and coupled with a tandem mass spectrometer (LC-ESI-MS/MS). A significant decrease in levels of docosahexaenoic acid and arachidonic acid in erythrocytes of diabetic patients with or without retinopathy was observed. The origin of this decrease was a loss of phosphatidyl-ethanolamine phospholipids esterified with these LCPUFAs. In diabetic patients without retinopathy, this change was balanced by an increase in the levels of several phosphatidyl-choline species. No influence of diabetes nor of diabetic retinopathy was observed on the concentrations of plasmalogen-type phospholipids.Conclusions and SignificanceDiabetes and diabetic retinopathy were associated with a reduction of erythrocyte LCPUFAs in phosphatidyl-ethanolamines. The increase of the amounts of phosphatidyl-choline species in erythrocytes of diabetic patients without diabetic retinopathy might be a compensatory mechanism for the loss of LC-PUFA-rich phosphatidyl-ethanolamines.
Highlights
Diabetic retinopathy (DR) is a microvascular complication of diabetes representing the first cause of blindness in the US and Europe before the age of 50 [1]
Diabetes and diabetic retinopathy were associated with a reduction of erythrocyte Long chain polyunsaturated fatty acids (LCPUFAs) in phosphatidyl-ethanolamines
The increase of the amounts of phosphatidyl-choline species in erythrocytes of diabetic patients without diabetic retinopathy might be a compensatory mechanism for the loss of LC-PUFA-rich phosphatidylethanolamines
Summary
Diabetic retinopathy (DR) is a microvascular complication of diabetes representing the first cause of blindness in the US and Europe before the age of 50 [1]. The activation of biochemical pathways by hyperglycemia, such as protein kinase C (PKC), aldolase-reductase and/or advanced glycation endproducts pathways, and oxidative pathways leads to retinal ischemia by extensive capillary abnormalities [2,3]. Long chain polyunsaturated fatty acids (LCPUFAs) including docosahexaenoic acid (DHA, C22:6n-3) and arachidonic acid (AA, C20:4n-6) are suspected to play key functions in the pathogenesis of diabetes as glucose and lipid metabolisms are closely related [5]. LCPUFAs from the n-3 family have been shown to inhibit many cellular and biochemical processes involved in the pathophysiology of DR, namely the PKC, aldolase reductase, and advanced glycation endproducts pathways, as well as the expression of VEGF, the loss of pericytes, and platelet aggregation [5]. Long chain polyunsaturated fatty acids (LCPUFAs) including docosahexaenoic acid and arachidonic acid are suspected to play a key role in the pathogenesis of diabetes. This study was aimed to highlight potential changes in the metabolism of phospholipids, and plasmalogens, and LCPUFAs at various stages of diabetic retinopathy in humans
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