Introduction: Tumor cells are characterized by abnormally accelerated energy metabolism. Therefore, inhibition of energy metabolism is considered a promising therapeutic target for cancer treatment. Glucose transporter (GLUT) is a uniporter protein which facilitates the transport of glucose in human cells. MicroRNAs (miRNAs) are small (20-22nt), tissue specific, non-coding RNA molecules which cause mRNA translational inhibition or degradation by binding to complementary target mRNAs. Global down-regulation of miRNA expression is an apparent feature of various human tumors, including Oral squamous cell carcinoma (OSCC). The aim of the study is to analyse the association of miRNA23a and Glucose transporters in diabetic OSCC Materials and methods: Samples of Control (n=5) , Precancerous tissue (n=5), Carcinoma tissue (n=5) were collected. miRNA was isolated from control and experimental samples using TRIR (total RNA isolation reagent) kit. Diluted RNA sample was quantified spectrophotometrically by measuring the absorbance (A) at 260/280 nm. RT-PCR is an approach for converting and amplifying a single stranded RNA template to yield abundant double stranded DNA products.The purpose of a PCR (Polymerase Chain Reaction) is to make a huge number of copies of a gene. 2X Reaction buffer, Forward primer, Reverse primer , cDNA- Template, Autoclaved milliQ water. Human GLUT 1 gene specific primers used were FW-5’-TGTGCAACCCATGAGCTAA-3’and RW-RW-5’ CCTGGTCTCATCTGGATTC-3’. Results:Overexpression of miRNA-23a was identified with increased fold change in OSCC. miRNA-23a promotes tumor cell differentiation and glucose metabolism in OSCC by acting as an upstream activator of GLUT1. Conclusion: miRNA-23a was identified to be up-regulated in OSCC. miRNA-23a may promote cancer cell proliferation and glucose uptake in OSCC by acting as an upstream activator of GLUT1.