Blood Cell Membranes Of Patients Research Articles

Studying fatty acid content in red blood cell membranes in diabetic retinopathy of type 2 diabetes patients

Introduction. Studying pathogenetic pathways that are formed under conditions of hyperglycaemia and trigger further metabolic changes resulting in diabetes complications over time are of special interest both in theoretical and practical medicine. Membrane of the red blood cell that stays in blood constantly and relatively durable is an obvious participant of all metabolic changes and cannot but reflect changes in metabolism. Objective: to study content of fatty acids (FAs) in red blood cell membranes of patients with diabetic retinopathy (DR) with type 2 diabetes (T2D). Materials and methods. The study enrolled 73 subjects maximally matched by age and gender: 50 patients with established long-lasting T2D complicated with DR and 23 patients in the control group. All the biochemical tests were performed at the certified laboratory under the standard methods. Gas chromatography was applied to study FA spectrum. Statistical analysis was performed in IBM SPSS Statistics 23. Results and discussion. The key difference between the lipid metabolism of patients with complicated long-lasting T2D and healthy subjects was a significant difference in FA content redistribution in the red blood cell membranes represented by increased “saturation”. The content of saturated FAs (SAFAs)in patients with DR was higher than in the CG: 1.5-fold for palmitic (С:16), 2-fold for myristic(С:14), pentadecanoic (С:15) and margaric (С:17) (Р < 0.05). The content of saturated stearic (С:18) FA was not changed significantly.The content of unsaturated FAs(USFAs) have changed multidirectionally: the content of linoleic (С18:2) and arachidonic (С20:4) decreased 1.5-1.7-fold, respectively. The content of linolenic (С18:3) increased 2-fold, and content of oleic FA (С18:1) was not changed significantly. Conclusion. Study of the fluctuations of FA levels in red blood cell membranesplays animportant role in the development of insulin resistance, T2D and its microvascular complicationsthat can be applied in creating treatment and prevention strategies ofDRin type 2 diabetes patients.

Fatty acid desaturation in red blood cell membranes of patients with type 2 diabetes is improved by zinc supplementation

Background/ObjectiveMembrane flexibility can be a determining factor in pathophysiological mechanisms of type 2 diabetes (T2D). As a cofactor of delta-5 desaturase (D5D) and delta-6 desaturase (D6D), and gene expression regulator, zinc may play a role modulating membrane flexibility by increasing membrane polyunsaturated fatty acids (PUFA) abundance. The objective of this study was to evaluate the effect of a 24-month zinc supplementation (30 mg elemental zinc) on membrane fatty acid composition in patients with T2D. Subjects/methodsSixty patients with T2D were evaluated. Thirty were randomly assigned to the zinc supplemented group and thirty to the placebo group. Fatty acid composition in red blood cell (RBC) membranes was determined by gas chromatography. Expression of gene encoding for D5D (FADS1), and D6D (FADS2) were evaluated in peripheral blood mononuclear cells by real-time polymerase chain reaction. ResultsAfter 24 months of supplementation, a greater abundance of docosapentaenoic acid (C22:5 n-3), arachidonic acid (C20:4 n-6), adrenic acid (C22:4 n-6), and total n-6 PUFA was found (p = 0.001, p = 0.007, p = 0.033, p = 0.048, respectively). The unsaturated fatty acids/saturated fatty acids ratio, and unsaturation index was increased in the zinc supplemented group at month 24 (p = 0.003 and p = 0.000, respectively). FADS1 gene was upregulated in the zinc group in relation to placebo at month 12 (p = 0.020). ConclusionsSupplementation with 30 mg/d elemental zinc during 24 months in patients with T2D had an effect on the composition of RBC membranes increasing PUFA abundance and in turn, improving membrane flexibility. This effect may be mediated by induction of D5D gene expression.

Significant decrease of saturation index in erythrocytes membrane from subjects with non-alcoholic fatty liver disease (NAFLD)

BackgroundThe lipidomic profiling of erythrocyte membranes is expected to provide a peculiar scenario at molecular level of metabolic and nutritional pathways which may influence the lipid balance and the adaptation and homeostasis of the organism. Considering that lipid accumulation in the cell is important in promoting tissue inflammation, the purpose of this study is to analyze the fatty acid profile in red blood cell membranes of patients with Non-Alcoholic Fatty Liver Disease (NAFLD), in order to identify and validate membrane profiles possibly associated with the degree of hepatic damage.MethodsThis work presents data obtained at baseline from 101 subjects that participated to a nutritional trial (registration number: NCT02347696) enrolling consecutive subjects with NAFLD. Diagnosis of liver steatosis was performed by using vibration-controlled elastography implemented on FibroScan. Fatty acids, extracted from phospholipids of erythrocyte membranes, were quantified by gas chromatography method.ResultsThe subjects with severe NAFLD showed a significant decrease of the ratio of stearic acid to oleic acid (saturation index, SI) compared to controls, 1.281 ± 0.31 vs 1.5 ± 0.29, respectively. Low levels of SI in red blood cell membranes, inversely associated with degree of liver damage, suggest that an impairment of circulating cell membrane structure can reflect modifications that take place in the liver. Subjects with severe NAFLDalso showed higher levels of elongase 5 enzymatic activity, evaluated as vaccenic acid to palmitoleic acid ratio.ConclusionsStarting from these evidences, our findings show the importance of lipidomic approach in the diagnosis and the staging of NAFLD.

Plasmalogen phospholipids in plasma lipoproteins of normolipidemic donors and patients with hypercholesterolemia treated by LDL apheresis

Recent evidence indicates that plasmalogen phospholipids are particularly sensitive to oxidation and may possess antioxidative properties. Approximately 4.4%–5.5% of phosphatidylcholine (PC), and 53%–60% of phosphatidylethanolamine (PE) consisted of the plasmalogen phospholipids, plasmenylcholine and plasmenylethanolamine, respectively, in whole plasma, low density lipoprotein (LDL) and high density lipoprotein (HDL) of 11 normolipidemic donors. Of total plasmalogen phospholipids in plasma, slightly more was associated with LDL particles (about 42%) than with HDL (36%). Plasmalogen phospholipid levels were analyzed in 12 patients with familial hypercholesterolemia (FH) regularly treated by LDL apheresis, of whom 6 were supplemented with vitamin E (alpha tocopherol, 400 IU/day), the remaining 6 not receiving the antioxidant. Before apheresis (pre), total plasmalogen phospholipid levels in plasma and LDL (expressed as μmol/mmol cholesterol of compartment) decreased as follows: patients receiving vitamin E > normolipidemia > patients not receiving vitamin E. In both hypercholesterolemic groups, the contents of plasmalogen phospholipids in whole plasma and LDL were 3–5-fold higher than those of vitamin E. Directly after apheresis (post), plasmalogen phospholipid levels in plasma were raised by about 50% in the two hypercholesterolemic groups, mostly due to increases in plasmenylethanolamine levels. Two days after apheresis (48 h post), plasmalogen contents were still elevated in plasma and red blood cell membranes of patients receiving vitamin E, while they had already reached pre-apheresis values in those not supplemented with alpha tocopherol. Molecular species of plasma diacyl phospholipids containing polyunsaturated fatty acids were elevated at pre in patients receiving vitamin E as compared to patients without supplementation. At 48 h post, LDL apheresis induced an increase in these molecular species only in patients receiving vitamin E. In conclusion, the contents of plasmalogen phospholipids in plasma lipoproteins are at least three times higher than those of vitamin E. LDL apheresis raises the level of plasmalogen phospholipids in plasma, the increase persisting longer in patients supplemented with vitamin E. Supplementation with vitamin E appears to protect plasmalogen phospholipids in plasma lipoproteins against oxidative degradation.

Composition of Phospholipid Fatty Acids in Red Blood Cell Membranes of Patients in Intensive Care Units: Effects of Different Intakes of Soybean Oil, Medium‐Chain Triglycerides, and Black‐Currant Seed Oil

Fatty acid composition of phospholipids in red blood cell membranes was studied in 32 severely head-injured or cerebral stroke patients receiving enteral nutrition for 3 weeks. During this study the effects of three diets differing only by their lipid composition were investigated. The daily energy intake of each patient amounted to 2950 kilocalories, of which the lipid fraction represented 45.7%. Diet A contained only soybean oil, diet B consisted of a 50% soybean oil and 50% medium-chain triglycerides mixture, and diet C was an emulsion of 50% soybean oil, 42.5% medium-chain triglycerides, and 7.5% black-currant seed oil. Our results showed no biochemical signs of fatty acid deficiency in red blood cell membranes for the patients at the beginning of the study, after a comparison with a control group of 20 healthy adults. Inhibition of delta 6-desaturase activity on linoleic acid (C18:2 omega 6) after diet A was suggested by an increase of linoleic acid without a corresponding increase of dihomo-gamma-linolenic acid (C20:3 omega 6). Replacing 50% of soybean oil by with medium-chain triglycerides (diet B) prevented this enzyme inhibition. Supply of black-currant seed oil rich in gamma-linolenic (C18:3 omega 6) and stearidonic (C18:4 omega 3) acids (diet C) induced significant increases of dihomo-gamma-linolenic and eicosapentaenoic (C20:5 omega 3) acids, without influencing arachidonic acid (C20:4 omega 6) levels. This balance was evaluated through the ratio (C20:3 omega 6 + C20:5 omega 3)/C20:4 omega 6.

699 INCREASED CHOLESTEROL SULFATE IN PLASMA AND RED BLOOD CELL MEMBRANES OF STEROID SULFATASE (STS) DEFICIENT PATIENTS

STS deficiency is an inborn error of metabolism due to a relatively common mutation on the short arm of the X chromosome. The phenotype of affected individuals includes decreased estriol production during fetal life and ichthyosis postnatally. Although increased levels of several steroid sulfates have been observed in amniotic fluid, maternal urine, and cord blood from such pregnancies, no consistent substrate abnormalities have been found beyond the perinatal period. Specifically, normal radioimmunoassayable plasma pregnenolone sulfate (PS), dehydroepiandrosterone sulfate (DS), and androstenediol sulfate (AS) have been reported. Utilizing gas chromatography (GC), we have found cholesterol sulfate (CS) to be strikingly elevated in plasma and red blood cell membranes of patients with STS deficiency. 80% methanol extracts were purified by solvent partition and TLC, subjected to solvolysis and quantitated by GC. Recoveries were monitored with 3H-CS. High levels of CS with normal levels of PS, DHEAS, and AS may indicate that desulfation is quantitatively more important for CS than for the other steroid sulfates. CS is known to affect membrane stability and the present observations may help to explain the pathogenesis of STS deficiency and X-linked ichthyosis.

The abnormal surface characteristics of the red blood cell membrane in congenital dyserythropoietic anaemia type II (HEMPAS).

The red blood cell membranes of patients with congenital dyserythropoietic anaemia Type II (CDA-II) were found to be abnormal. They had altered antigenic characteristics, decreased electrophoretic mobility, decreased sialic acid content, and abnormal filtration through polycarbonate filters. Proteins extracted from the CDA-II erythrocytes showed a different banding pattern on polyacrylamide gels compared to normal erythrocytes. Erythrocytes from clinically unaffected siblings and parents showed similar but less striking abnormalities of antigenic surface characteristics and banding patterns on polyacrylamide gels with nearly normal surface charge, sialic acid content, and filtration properties. These studies suggest a correlation between the degree of membrane abnormality and the clinical state of the CDA-II family member, demonstrate the erythrocyte in the heterozygote state is not normal, and support the concept of CDA-II as an autosomal recessive disease.