Abstract
(1) Background: Chemerin, or the RARRES2 (Retinoic Acid Receptor Responder 2) gene, is found to be associated with an increased incidence of insulin resistance, endothelial dysfunction, type 2 diabetes (T2D), and coronary artery disease (CAD). This study investigates associations of RARRES2 rs17173608 with insulin resistance and the severity of CAD in non-obese T2D patients in relation to the clinical and genetic factors. (2) Methods: A total of 300 patients with T2D and CAD were recruited in this study. The associations of insulin resistance and the severity of CAD with RARRES2 rs17173608 and clinical factors were assessed. The genotyping procedures were performed using the TaqMan method. The significant associations (p ≤ 0.05) from preliminary tests were employed to carry out the secondary analysis. (3) Results: RARRES2 rs17173608 (TT, TG, and GG polymorphisms in the preliminary analysis; TG and GG polymorphisms in a secondary analysis) was associated with insulin resistance and the severity of CAD in both the preliminary and secondary analysis (all p-values were < 0.05). Additionally, in the secondary analysis, FPG and ACEI were also associated with insulin resistance and the severity of CAD (all p-values were < 0.05). (4) Conclusion: From the preliminary findings, rs17173608 is a significant predictor of insulin resistance and the severity of CAD.
Highlights
Published: 23 May 2021Chemerin, known as retinoic acid receptor responder protein 2 (RARRES2) and tazarotene50 induced gene 2 [1], is a chemoattractant protein involved in the pathogenesis of metabolic syndrome [2]
(4) Conclusion: From the preliminary findings, rs17173608 is a significant predictor of insulin resistance and the severity of coronary artery disease (CAD)
The preliminary and secondary analyses revealed that the TG and GG polymorphisms of rs17173608 were significantly associated with insulin resistance and the severity of CAD
Summary
Known as retinoic acid receptor responder protein 2 (RARRES2) and tazarotene induced gene 2 [1], is a chemoattractant protein involved in the pathogenesis of metabolic syndrome [2]. It is secreted in the liver, acts as a chemotactic agent, and is highly stimulated by elements of the innate immune system, such as plasmacytoid dendritic cells and macrophages [2]. Chemerin induces angiogenesis of endothelial cells and results in endothelial dysfunction [3]. With 16–25% of variations ascribed to genetic factors [5]
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