Background: Alteration of the gut microflora leads to local intestinal inflammation which produces various primary and secondary metabolites that cause chronic inflammation, leading to metabolic syndrome. Objectives: To determine the gut microbiome about biochemical and inflammatory markers in type 2 diabetes patients and to assess the clinical outcomes of metabolic syndrome for gut microbiota composition. Methods: In this hospital-based observational study, 41 type 2 diabetes mellitus patients were included and underwent clinical examination. The gut microbiome diversity was detected from stool samples through DNA extraction followed by 16s RNA gene sequencing and bioinformatical analyses. Using blood samples, the immune response analysis was also done by identifying CD4+T cells through blood immune cells analysis. Results: After gene sequencing from stool samples, the gut microbiota species of rumonicoccus, fusobacterium, and blautia were identified among 9(42.9%), 9(42.9%), and 10(47.6%) patients only in the case group. However, fecalibacterium prasunitzii, bifidobacterium, akkermansia mucinphila and bacteriodes fragilis were 1(5%), 2(10%), 10(50%) patients only in the control group. In both groups, lactobacillus, and escherichia coli were seen among 3(15%) and 20(100%) patients in the control group, followed by 4(19%) and 20(95.2%) patients in the type 2 diabetes group. The incidence of metabolic syndrome was seen in 4(20%) patients in the control group and it was in 19(90.5%) patients in the case group where the prevalence of metabolic syndrome was significantly higher in the type 2 diabetes group than the control group (Fisher’s Exact Test, P=0.001). Conclusion: Among the studied population, the gut microbiota was found to be significantly different in the diabetics when compared to non-diabetics and helped to identify the bacteria that were important in the development of diabetes. The elevation of inflammatory markers further showed the possible role of gut microbiota in creating a state of chronic inflammation in these patients, ultimately leading to insulin resistance and the development of type 2 diabetes mellitus.