Abstract

Objective: Diabetes Mellitus, specifically Type 2 Diabetes Mellitus which accounts for almost 90% of all diabetes, has emerged as one of the biggest pandemics of modern times. Investigations are underway, with different areas of focus due to the disease’ heterogeneity. This review paper will go through some research which has been done to illustrate the role of Vitamin A in the control of hyperglycemia in T2DM.
Methods: An online Literature search was done using electronic databases from MedLine, PubMed, Google Scholar and ResearchGate published mostly in the years 2014-2019.
Result: Retinol binding protein levels especially of RBP4 was found to be positively associated with insulin resistance which was elucidated by the mechanism of low glucose uptake in skeletal muscles and enhanced gluconeogenesis in the liver of mice. Furthermore, the antioxidant property of Vitamin A was also given focus due to the fact that hyperglycemia in T2DM result to oxidative stress because of production of reactive oxygen species (ROS). Another novel mechanism of Vitamin A’s ability to control hyperglycemia in T2DM as demonstrated by retinol supplementation in animal studies’ is the suppression of retinoid-x-receptor resulting to decreased adipogenesis, with consequent improved insulin sensitivity. The other mechanisms include the following:
a) low Vitamin A level demonstrated diminished islet cells due to induced cellular stressmediated apoptosis and reducing steatoryl-CoA desaturase 1-mediated oleic acid (SCD1) synthesis.
b) vitamin A showed slight increase in GLUT4 expression causing increase in glucose uptake in skeletal muscles and adipocytes.
Conclusion: The different biochemical bases of how Vitamin A level affects insulin sensitivity/resistance through its antioxidant property, expression of GLUT4 transport protein for enhanced muscle and adipose glucose uptake, and decreased adipogenesis/lipogenesis provide strong evidence on its important role in the control of hyperglycemic state in T2DM.

Keywords:Diabetes mellitus; Metabolic disease; Hyperglycemia; Dyslipidemia; Nutrition; Vitamins C; Vitamin A

Abbreviations: AGE: Advanced Glycation End-product; CHOP, C/EBP: Homologous Protein; CVD: Cardiovascular Disease; IL: Interleukin; IRS: Insulin Receptor Substrate; OXPHOS: Oxidative Phosphorylation; PERK: Protein Kinase R-Like Endoplasmic Reticulum Kinase; PKC: Protein Kinase C; ROS: Reactive Oxygen Species; SOCS: Suppressor of Cytokine Signaling; SOD: Superoxide Dismutase; T2DM: Type 2 Diabetes Mellitus; TNF: Tumor Necrosis Factor.