Asian Journal of Advances in Research

Diabetes mellitus and liver cirrhosis interact bidirectionally, but their coexistence creates a clinical state that cannot be managed safely by applying conventional diabetes algorithms without modification. Cirrhosis alters insulin clearance, hepatic glucose production, glycogen storage, skeletal-muscle glucose disposal, nutritional status and drug handling, while diabetes and insulin resistance may contribute to portal-hypertensive complications, hepatic encephalopathy, cardiovascular and renal risk, and mortality. The purpose of this critical narrative review is to integrate current concepts in diabetes phenotyping, diagnosis, monitoring and treatment across compensated and decompensated cirrhosis, with particular attention to newer glucose-lowering therapies. Literature published principally from 2000 to 17 July 2026 was evaluated, with older seminal studies retained where necessary. The evidence indicates that hepatogenous diabetes remains a useful pathophysiological construct but lacks validated diagnostic criteria that reliably separate it from pre-existing type 2 diabetes. Glycated haemoglobin and fasting glucose may underestimate dysglycaemia in advanced cirrhosis; oral glucose tolerance testing, structured capillary monitoring and, in selected patients, continuous glucose monitoring can therefore add clinically important information. Treatment priorities shift as liver disease advances: avoidance of hypoglycaemia, preservation of nutritional and functional reserve, prevention of acute kidney injury and adaptation to cognitive impairment become increasingly important. Metformin has the strongest observational evidence for safety and possible survival benefit in stable compensated cirrhosis when contraindications are absent. Glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors are supported by encouraging observational data in compensated disease and by metabolic benefits relevant to metabolic dysfunction-associated steatotic liver disease, but evidence in decompensated cirrhosis remains limited. Insulin remains indispensable during severe decompensation and acute illness despite substantial hypoglycaemia risk. The central management principle is therefore stage-specific, multidisciplinary treatment that distinguishes metabolic benefit from liver-specific evidence and calibrates therapeutic intensity to hepatic reserve, renal function, nutrition and hypoglycaemia vulnerability.