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REVIEW ARTICLE
Year : 2020  |  Volume : 4  |  Issue : 2  |  Page : 95-107

The associations between retinol binding protein-4 and cardiometabolic profile: Intertwined-intricate relationship


Department of Pharmacology, Toxicology and Medicine, College of Medicine Almustansiriya University, Baghdad, Iraq

Correspondence Address:
Prof. Hayder Mutter Al-Kuraishy
Department of Pharmacology, Toxicology and Medicine, College of Medicine Almustansiriya University, P.O. Box 14132, Baghdad
Iraq
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bbrj.bbrj_6_20

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Retinol binding protein-4 (RBP4) is a new adipokine synthesized by the liver and adipose tissue, and its secretion depends on retinol concentrations and reflects visceral fat mass. RBP4 serum levels are regarded as a new biomarker in follow-up and diagnosis of overweight and obesity and other cardiometabolic disorders, such as hypertension, ischemic stroke, and dyslipidemia. Different drugs such as statins, fibrates, glucagon-like peptide 1 (GLP-1), dipeptidyl peptidase-IV (DPPIV) inhibitors, and thiazolidinediones (TZDs) have been reported to reduce RBP4 levels. The objectives of the present study were to illustrate the role of RBP4 in different cardiometabolic disorders and to explore the conflicting about the effect of different drug groups on the circulating RBP4 levels. A multiplicity of search strategies took on and assumed which included electronic database searches of Scopus, Web of Science, Medline, Cochrane Central Register of Controlled Trials, and PubMed using MeSH terms, keywords, and title words during the search. RBP4 plasma levels are mainly correlated with visceral adiposity and less to the subcutaneous adipose tissue. Statins may reduce or increase RBP4 plasma levels. Fibrate drugs, TZDs, DPPIV inhibitors, and GLP-1 agonists reduce RBP4 plasma levels through suppression of adipose tissue RBP4 mRNA and elevation of adiponectin levels. Metformin reduces circulating RBP4 levels through the improvement of insulin sensitivity, upregulation of glucose transporter 4 (GLUT4), and activation of adipocytes PPARα.


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