T-cadherin status among negrito aborigines and its association with metabolic syndrome and atherogenesis / Andrian Alif Faisal

• Main Author: Faisal, Andrian Alif
• Format: Thesis
• Language: English
• Published: 2019
• Subjects: Pathologic pigmentation
• Online Access: https://ir.uitm.edu.my/id/eprint/88872/1/88872.pdf; https://ir.uitm.edu.my/id/eprint/88872/
• Institution: Universiti Teknologi Mara

Introduction: T-cadherin is hypothesized to provide cardioprotection by mediating the anti- atherogenic effects of adiponectin. Previous studies have shown strong expression of the CDH13 gene which encodes for T-cadherin, among the Negrito aborigines. This study aimed to determine the status of T-cadherin in this population, as well as its association with biomarkers of coronary risk, traditional risk factors for coronary artery disease (CAD) and individual components of metabolic syndrome (MS). Materials & Methods: This cross-sectional study recruited 150 Negritos (the minimum samples size was established at 120 based on the OpenEpi Sample Size Calculator, with a confidence level of 80% and prevalence of high Framingham risk score among inland aborigines at 25%). The limited sample size is attributable to the small total population of the Negrito aborigines (estimated at 4500), as well as their remote living areas which made access to them a challenge. Demographic data was collected by way of interview questionnaire and physical examination. Cardiometabolic parameters analysed included total cholesterol (TC), triglyceride (TG) and high density lipoprotein cholesterol (HDL-c) concentrations which were measured by enzymatic reference methods on an automated analyser (Cobas 400 PLUS, Roche Diagnostics, Germany). Low density lipoprotein cholesterol (LDL-c) concentrations were derived by calculation using the Friedewald equation. Plasma glucose was analysed by hexokinase method on an automated platform (Cobas Integra 400, Roche Diagnostics, Germany). Serum hsCRP and Lp(a) concentrations were analysed on an automated Cobas 400 PLUS analyser (Roche Diagnostics, Germany), while T-cadherin and sICAM-1 were analysed by ELISA (Wuhan Fine Biological Technology Co.,Ltd., Hubei, China and eBioscience Bender MedSystems, Vienna, Austria, respectively). Results: An inverse correlation was observed between T-Cadherin and sICAM-1 concentrations (r=-0.447, p=0.01). There was no association between T-cadherin and Lp(a) or hsCRP concentrations. No significant correlation was seen between T-cadherin and individual components of MS either. Discussion: These observations suggest that T-cadherin could possibly have some influence in ameliorating endothelial activation. They also suggest that T-cadherin levels are genetically determined and are mostly unaffected by traditional risk factors for CAD. However, future studies involving larger sample size would further strengthen these observations and help to identify the specific anti-atherogenic mechanism to which T-cadherin contributes, as well as its potential role in risk stratification strategies for coronary artery disease.