Metabolic-dysfunction-associated steatotic liver disease (MASLD) and type 2 diabetes mellitus (T2DM) share insulin-resistance-driven metabolic derangements that promote hepatic steatosis, systemic inflammation, and fibrogenesis. MASLD affects approximately 65% of adults with T2DM, with nearly half meeting histologic criteria for metabolic-dysfunction-associated steatohepatitis (MASH), significantly increasing the risk for cirrhosis, hepatocellular carcinoma, and cardiovascular events. Key pathophysiologic mechanisms include upregulated de novo lipogenesis, impaired β-oxidation, and lipotoxic signaling cascades, establishing a bidirectional relationship in which MASLD worsens glycemic control and T2DM accelerates fibrotic progression. Randomized clinical trials have shown that glucagon-like peptide-1 (GLP-1) receptor agonists reduce hepatic fat fraction by approximately 20% to 40% and improve aminotransferase levels, while sodium-glucose cotransporter 2 inhibitors achieve modest reductions in steatosis with additional cardiometabolic benefits; extending these metabolic effects into histologic disease modification, semaglutide has become the first GLP-1 receptor agonist to receive US Food and Drug Administration accelerated approval for anti-fibrotic benefit in MASH, based on fibrosis improvement demonstrated in the phase 3 ESSENCE trial among adults with moderate-to-advanced fibrosis (F2–F3) without cirrhosis, thereby establishing its role beyond metabolic control as a disease-modifying therapy. Dual and triple incretin agonists yield additive improvements in glycemic and hepatic endpoints in early disease, although histologic antifibrotic efficacy remains unproven. In advanced fibrosis, phase II and III trials of agents targeting apoptosis-signal-regulating kinase 1, farnesoid X receptor, and fibroblast growth factor 21 pathways have produced mixed results, emphasizing the need for more effective therapies. Integration of validated noninvasive fibrosis assessment (eg, fibrosis-4 index with transient elastography), sustained weight loss of ≥10%, evidence-based antidiabetic pharmacotherapy, and timely enrollment in clinical trials within multidisciplinary care frameworks offers the greatest potential to modify the MASLD-T2DM disease trajectory and improve long-term outcomes.