Background: Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by insulin resistance and hyperglycaemia. Insulin resistance involves reduced tissue responsiveness to insulin, disrupting glucose metabolism and contributing to T2DM. Dyslipidaemia and chronic inflammation exacerbate this condition, heightening cardiovascular risk. This study investigates the biochemical basis of insulin resistance and its implications for T2DM progression. Methods: A cross-sectional study was conducted on 200 participants, comprising 100 T2DM patients and 100 non-diabetic controls. Data on demographics, BMI, and family history were collected. Biochemical markers, including fasting plasma glucose, HbA1c, insulin levels, lipid profile, and inflammatory markers (TNF-α, IL-6), were analysed. Insulin resistance was assessed using HOMA-IR. Statistical analyses included t-tests, Pearson’s correlations, and multivariate regression. Results: T2DM patients exhibited significantly higher fasting plasma glucose (165 ± 40 vs. 90 ± 10 mg/dL), HbA1c (8.5 ± 1.2 vs. 5.2 ± 0.5%), and HOMA-IR (4.5 ± 1.2 vs. 1.4 ± 0.4) compared to controls (p < 0.001). Dyslipidaemia was evident with elevated triglycerides (180 ± 40 vs. 120 ± 25 mg/dL) and LDL-C (130 ± 30 vs. 100 ± 20 mg/dL) but lower HDL-C (42 ± 7 vs. 55 ± 10 mg/dL). TNF-α and IL-6 levels were markedly higher in T2DM patients. BMI and fasting glucose emerged as significant predictors of insulin resistance. Conclusion: This study highlights the interplay of glucose dysregulation, lipid abnormalities, and chronic inflammation in T2DM. Targeted interventions addressing obesity, glycemic control, and inflammation are critical for effective management and cardiovascular risk reduction.