Evaluation of paraoxonase-1 activity in Yemeni Type 2 diabetes mellitus and its association with atherogenic risk factors

Ekram Al-Eryani *, Abdul-Kafi Shuga’a Al-Dini, Farooq Hayel, Munira Dughish

1Department of Molecular Medicine, Faculty of Medicine, University of Malaya

Department of Biochemistry and Molecular Biology, Faculty of Medicine and Health Sciences, University of Sana`a, Sana`a, Yemen

SUJMS • 2021 | Jane | Vol 15| Issue. (1))

Introduction:


Diabetes mellitus (DM) is a group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, and or both. The chronic hyperglycemia of diabetes is associated with long-term damage, failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels [1]. Type 2 DM is caused by insulin resistance, inadequate secretion of insulin, is generally associated with overweight and obesity [2].

The paraoxonase (PON) enzyme family is constituted by three members: PON1, PON2, and PON3. Paraoxonase-1 (PON1) is the most studied member of the paraoxonase family and is classified as an aryldialkylphosphatase [3]. Paraoxonase-1 is a 44 kD calcium-dependent glycoprotein

synthesized by the liver and associated with high-density lipoprotein (HDL) contributes to the lipoprotein functionality [4-6]. It has been widely demonstrated that PON1 protects HDL, low-density lipoprotein (LDL), endothelial cells, and intimal macrophages from oxidative insult [3,7]. This protective action occurs via hydrolysis of the potential physiological substrate, lipo-lactones, which originate from the oxidative damage of phospholipids present on cell and lipoprotein surfaces [8]. Low PON1 activity has been reported to increase the development of atherosclerosis [9]. Nonetheless, the evidence of differential expression of PON1 in the context of Type 2 DM is still unclear. The recognized evidence about PON1 expression in Type 2 DM is related to its genetic polymorphisms, which have

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