Abstract
Fatty acid (FA) profiles in the plasma of patients with metabolic syndrome and chronic kidney disease (CKD) seem to be identical despite their different etiology (dietary mistakes vs. cachexia). The aim of this study was to compare both profiles and to highlight the differences that could influence the improvement of the treatment of patients in both groups. The study involved 73 women, including 24 patients with chronic kidney disease treated with haemodialysis, 19 patients with metabolic syndrome (MetS), and 30 healthy women in the control group. A total of 35 fatty acids and derivatives were identified and quantified by gas chromatography. Intensified elongation processes from acid C10:0 to C16:0 were noted in both groups (more intense in MetS), as well as an increased synthesis of arachidonic acid (C20:4n6), which was more intense in CKD. Significant correlations of oleic acid (C18:1n9), gamma linoleic acid (C18:3n6), and docosatetraenoate acid (C22:4n6) with parameters of CKD patients were observed. In the MetS group, auxiliary metabolic pathways of oleic acid were activated, which simultaneously inhibited the synthesis of eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) from alpha lipoic acid (ALA). On the other hand, in the group of female patients with CKD, the synthesis of EPA and DHA was intensified. Activation of the synthesis of oleic acid (C18: 1n9 ct) and trans-vaccinic acid (C18:1) is a protective mechanism in kidney diseases and especially in MetS due to the increased concentration of saturated fatty acid (SFA) in plasma. The cause of the increased amount of all FAs in plasma in the CKD group, especially in the case of palmitic (C16:0) and derivatives stearic (C18:0) acids, may be the decomposition of adipose tissue and the progressing devastation of the organism, whereas, in the MetS group, dietary intake seems to be the main reason for the increase in SFA. Moreover, in MetS, auxiliary metabolic pathways are activated for oleic acid, which cause the simultaneous inhibition of EPA and DHA synthesis from ALA, whereas, in the CKD group, we observe an increased synthesis of EPA and DHA. The higher increase of nervonic acid (C24:1) in CKD suggests a higher degree of demyelination and loss of axons.
Highlights
Fatty acids (FAs) in kidney diseases are sporadically described in the literature
When comparing the profile of FA between metabolic syndrome (MetS) and CG, a significant decrease was determined in the percentage of acids from caprylic (C8:0) to myristylic acid (C14:1) in MetS
It was determined that saturated fatty acids (SFA) such as C16:0 and C18:0 are responsible for increased lipotoxicity, insulin resistance, and cell death via apoptosis [4]
Summary
Fatty acids (FAs) in kidney diseases are sporadically described in the literature. It is known that the changes in the fatty acids of plasma contribute to lipotoxicity and the accumulation of excessive lipids in kidneys, which is a factor facilitating the development and progress of kidney disease, especially in the case of accompanying obesity and diabetic nephropathy (DN) [1]. Lipotoxicity seems to be an adaptive process that enables the podocytes, for a short time, to cope with increased levels of fatty acids (FA) [3] When this buffering mechanism becomes overloaded, lipotoxicity together with insulin resistance and endoplasmic reticulum (ER) stress may lead to the death of a podocyte, which contributes to the progress of the disease [3,4]. Despite the various pathogeneses of the diseases, we were interested in whether the inflammatory process accompanying both diseases has a similar course, and whether inflammatory mediators synthesized inter alia with arachidonic acid will cause a similar cascade of changes in the profile of free fatty acids (FFA) Because both CKD and MetS may have a different etiology, we decided to determine the differences in FA contents between the profiles of patients in both diseases. We hope that our study may contribute to the explanation of the mechanisms and the increase of the activity of metabolic processes in both diseases
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