Crucial Interactions between Altered Plasma Trace Elements and Fatty Acids Unbalance Ratio to Management of Systemic Arterial Hypertension in Diabetic Patients: Focus on Endothelial Dysfunction

Author:

Gouaref Ines12,Otmane Amel3,Makrelouf Mohamed3,Abderrhmane Samir Ait4,Haddam Ali El Mahdi5,Koceir Elhadj-Ahmed12ORCID

Affiliation:

1. Bioenergetics and Intermediary Metabolism Team, Laboratory of Biology and Organism Physiology, Biological Sciences Faculty, Nutrition and Pathologies Post Graduate School, Houari Boumediene University of Sciences and Technology (USTHB), Bab Ezzouar, Algiers 16123, Algeria

2. Tamayouz Laboratory, Centre de Recherche en Biotechnologie (CRBT), Ali Mendjli Nouvelle Ville UV 03 BP E73, Constantine 25000, Algeria

3. Biochemistry and Genetics Laboratory, University Hospital Center, Mohamed Lamine Debaghine, Bab El Oued, Algiers 16000, Algeria

4. Diabetology Unit, University Hospital Center, Mohamed Seghir Nekkache (ex. HCA de Aïn Naâdja), Algiers 16208, Algeria

5. Diabetology Unit, University Hospital Center, Mohamed Lamine Debaghine, Algiers I-University, Bab El Oued, Algiers 16000, Algeria

Abstract

The coexistence of SAH with T2DM is a common comorbidity. In this study, we investigated the link between altered plasma antioxidant trace elements (ATE: manganese, selenium, zinc, and copper) and fatty acids ratio (FAR: polyunsaturated/saturated) imbalance as transition biomarkers between vascular pathology (SAH) to metabolic pathology (T2DM). Our data revealed strong correlation between plasma ATE and FAR profile, which is modified during SAH-T2DM association compared to the healthy group. This relationship is mediated by lipotoxicity (simultaneously prominent visceral adipose tissue lipolysis, significant flow of non-esterified free fatty acids release, TG-Chol-dyslipidemia, high association of total SFA, palmitic acid, arachidonic acid, and PUFA ω6/PUFA ω3; drop in tandem of PUFA/SFA and EPA + DHA); oxidative stress (lipid peroxidation confirmed by TAS depletion and MDA rise, concurrent drop of Zn/Cu-SOD, GPx, GSH, Se, Zn, Se/Mn, Zn/Cu; concomitant enhancement of Cu, Mn, and Fe); endothelial dysfunction (endotheline−1 increase); athero-thrombogenesis risk (concomitant rise of ApoB100/ApoA1, Ox-LDL, tHcy, and Lp(a)), and inflammation (higher of Hs-CRP, fibrinogen and ferritin). Our study opens to new therapeutic targets and to better dietary management, such as to establishing dietary ATE and PUFA ω6/PUFA ω3 or PUFA/SFA reference values for atherosclerotic risk prevention in hypertensive/diabetic patients.

Funder

Tamayouz Laboratory, Centre de Recherche en Biotechnologie (CRBT), Ali Mendjli Nouvelle Ville UV 03 BP E73, Constantine, Algeria

Publisher

MDPI AG

Reference225 articles.

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