Abstract

ObjectiveThe aim of this study was to determine the role of serum prolidase activity and the possible association with oxidative stress parameters in non-diabetic metabolic syndrome.Methods30 obese patients without metabolic syndrome (MetS), 34 non-diabetic obese patients with MetS, and 23 volunteer control subjects were enrolled in the study. Fasting plasma glucose (FPG), plasma glucose following 75 g glucose administration, high-density lipoprotein- cholesterol (HDL-C), high-density lipoprotein- cholesterol (LDL-C), total cholesterol, triglyceride (TG), total antioxidant status (TAS), total oxidative status (TOS), oxidative stress index (OSI), and prolidase activities of all subjects were analyzed.ResultsProlidase levels was significantly higher in MetS group compared to both obese and control groups (p < 0.001 and p < 0.05 respectively). Prolidase was also higher in the obese group than in the control group (p < 0.05). Prolidase was negatively correlated with TAS and HDL-C (r = −0,362, p < 0.001; r = −0.320, p < 0.01, respectively) and positively correlated with BMI, weight, waist-c, SBP, DBP, TG, TC, LDL-C.ConclusionProlidase activity may have a role in the pathogenesis of metabolic syndrome.

Highlights

  • Metabolic syndrome (MetS) is defined as the existence of obesity, insulin resistance, glucose intolerance, hypertension, and dyslipidemia [1]

  • Systolic blood pressures (SBP), diastolic blood pressures (DBP) and TG levels were significantly higher in the MetS group compared to both obese and control groups (Table 1)

  • Prolidase levels were significantly higher in MetS group compared to both obese and control groups (p < 0.001 and p < 0.05respectively) and in the obese group compared to the control group (p < 0.05)

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Summary

Introduction

Metabolic syndrome (MetS) is defined as the existence of obesity, insulin resistance, glucose intolerance, hypertension, and dyslipidemia [1]. Subjects with MetS may be obese but all obese patients may not have MetS. Both MetS and obesity have been shown to have impacts on cardiovascular mortality and morbidity [2]. Endothelial disfunction causes alterations in the arterial vasculature and leads to micro- and macrovascular complications. The remodelling of the endothelial basal membrane, resulted with erosion and thrombosis, increases the oxidative stress and alters matrix metalloproteinases (MMPs) expression [3]. A member of the MMP family, is a cytosolic imidodipeptidase, which splits imidodipeptides with C-terminal proline or hydroxyproline. The enzyme plays an important role in the recycling of proline from imidodipeptides for resynthesis of collagen and other proline containing proteins [4].

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