Platelet-rich plasma (PRP) is proven a cost-effective therapeutic choice for different ailments. The current study was designed to highlight the effects of heterologous platelet-rich plasma (PRP) on deteriorated hepatic tissues and impaired glucose metabolism in alloxan-induced diabetic mice. A total of thirty (30) male mice were selected and grouped as control (CG), PRP group (PG), diabetic group (DG), treated group 1 (T1G), and treated group 2 (T2G). PG was given a subcutaneous dose of PRP (0.5 ml/kg body weight) twice a week for four weeks. DG, T1G, and T2G were first given a single dose of alloxan intraperitoneally (150 mg/kg) to induce diabetes. PRP (0.5 ml/kg body weight) was given twice a week to T1G and T2G for two and four weeks respectively. After four weeks, all the mice were sacrificed to excise liver for histological observations and gene expression analysis. Hepatic histo-morphological analysis revealed ballooning of hepatocytes, dilatation of sinusoids, and collagen deposition in the alloxan-induced diabetic group (DG) and it was significantly reduced in both T1G and T2G. Additionally, a significant change in the expression of several hepatic genes was observed. Fbp1, G6pc, and Pklr showed an upregulation while a downregulation was detected in the expression of Pck1 in DG. A significant restoration was observed in Fbp1, and G6pc after PRP treatment but no change was observed in Pklr expression. Genes of glycolytic pathway, Hk1 and Gck, were downregulated significantly in DG compared to CG and PRP treatment restore the expression in both treated groups T1G and T2G. Moreover, Wnt2, Wnt4, and Wnt9a genes of the Wnt signaling pathway were also upregulated in DG, conversely, downregulate in T1G and T2G. No significant change in expression of Wnt5b and Wnt9b was observed in DG compared to control. Current study revealed that PRP anticipates a reduction in glucose production and glucose consumption by ameliorating hepatic tissue and modulating the glucose metabolism. So, it may use as one of the adjunctive therapies to treat T2DM in future but further more detailed investigations are suggested.