Iis Isnayati, Nurjannah Achmad, Salma Andintama

BLOOD GLUCOSE LEVELS ARE STRONGLY ASSOCIATED WITH VCAM-1 LEVELS IN PATIENTS WITH METABOLIC SYNDROME

Introduction

Blood glucose levels are strongly associated with vcam-1 levels in patients with metabolic syndrome. Strong association found between blood glucose, triglycerides, and VCAM-1 in metabolic syndrome patients. Insights into endothelial dysfunction and cardiovascular risk.

Abstract

Metabolic syndrome is a combination of metabolic risk factors that cause cardiovascular disease. These risk factors include high blood pressure, obesity, low HDL levels, hyperglycemia, and hypertriglyceridemia. This study aims to investigate the relationship between the components of metabolic syndrome and VCAM-1 levels, a marker of endothelial dysfunction, in patients with metabolic syndrome residing in RW 01 Cibeber, Cimahi. The study was conducted using a cross-sectional design with analytical descriptive methods. The respondents were 44 people who were taken by consecutive sampling. The components of the metabolic syndrome based on the NCEP ATP-III criteria include waist circumference, blood pressure, triglyceride levels as measured by the colorimetric GPO-PAP (Glycerol Peroxidase Phosphate Acid) enzymatic test, fasting blood glucose levels using the GOD-PAP (Glucose Aminoantypirin Oxidase-Peroxidase), and HDL cholesterol levels with the Trinder PEG (Polyethylene Glycol) precipitation method. VCAM-1 levels were examined using a quantitative enzyme-linked immunosorbent assay method as a marker of endothelial dysfunction. The results showed that most subjects had three or more of the five components (50%), and more than half of the subjects had high levels of VCAM-1 (63.6%). In addition, there was a significant relationship between the two components of the metabolic syndrome and VCAM-1 levels, namely fasting blood sugar (p = 0.000; r = 0.570) and triglycerides (p = 0.001; r = 0.501). Increased blood sugar causes changes in insulin signaling, interfering with NO production and increasing pro-inflammation, which in turn increases VCAM-1. At high triglyceride levels, it causes oxidative stress, leading to damage to vascular tissue, which in turn increases VCAM-1 DOI : 10.54052/jhds/v5n2.p199-212

Review

This study investigated the crucial relationship between components of metabolic syndrome and levels of VCAM-1, a marker of endothelial dysfunction, in a specific patient cohort. The chosen area of inquiry is highly relevant given the increasing global prevalence of metabolic syndrome and its strong association with cardiovascular disease. The abstract clearly outlines the study's aim and utilizes a cross-sectional design to assess the prevalence of MetS components and their associations with VCAM-1. The finding that a significant proportion of subjects exhibited multiple MetS components and high VCAM-1 levels underscores the significant cardiovascular risk present in this population. The principal conclusion, highlighting the strong association of fasting blood glucose and triglycerides with elevated VCAM-1, provides valuable insight into specific drivers of endothelial dysfunction within the metabolic syndrome context. Methodologically, the study employed appropriate and recognized techniques for assessing metabolic syndrome components (NCEP ATP-III criteria) and biochemical markers. The use of established enzymatic and ELISA methods for measuring triglycerides, fasting blood glucose, HDL cholesterol, and VCAM-1 lends credibility to the reported results. The statistical analysis revealing highly significant positive correlations (p < 0.001) for both fasting blood sugar (r = 0.570) and triglycerides (r = 0.501) with VCAM-1 levels is a key strength, indicating robust associations. Furthermore, the abstract offers plausible mechanistic explanations, linking hyperglycemia to insulin signaling disruption, reduced NO production, and increased pro-inflammation, and hypertriglyceridemia to oxidative stress, both ultimately converging on increased VCAM-1 expression. While the findings are compelling, some limitations warrant consideration. The cross-sectional design inherently prevents the establishment of causality, meaning that while associations are strong, the temporal sequence of events cannot be definitively determined. The sample size of 44 respondents, while sufficient for detecting the reported strong correlations, is relatively small and drawn from a very specific geographic location (RW 01 Cibeber, Cimahi), which may limit the generalizability of the findings to broader populations. Future research would benefit from larger, multi-center studies and, ideally, longitudinal designs to track changes in VCAM-1 in response to metabolic interventions and to provide stronger evidence for causal relationships. Nevertheless, this study reinforces the critical importance of managing hyperglycemia and dyslipidemia as key strategies to mitigate endothelial dysfunction and reduce cardiovascular risk in patients with metabolic syndrome.

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