ANATOMICAL AND PHYSIOLOGICAL CHANGES IN THE HUMAN LIVER IN DIABETES MELLITUS

Diabetes mellitus represents a chronic metabolic disorder that profoundly disrupts hepatic carbohydrate, lipid, and protein metabolism, resulting in a spectrum of anatomical and physiological alterations in the liver. Chronic hyperglycemia and insulin resistance trigger excessive de novo lipogenesis, influx of free fatty acids, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum stress, and activation of inflammatory and fibrogenic pathways. These processes culminate in hepatic steatosis, progression to metabolic dysfunction-associated steatohepatitis (MASH), ballooning degeneration, Mallory-Denk bodies, perisinusoidal fibrosis, and ultimately cirrhosis with increased risk of hepatocellular carcinoma. The review comprehensively analyzes bidirectional pathophysiological links between diabetes and metabolic dysfunction-associated steatotic liver disease (MASLD), ultrastructural and histopathological changes, molecular signaling cascades (IRS/PI3K/Akt, SREBP-1c, NF-κB, TGF-β), and clinical implications for both type 1 and type 2 diabetes. Emphasis is placed on the central role of the liver in perpetuating systemic metabolic derangement and the necessity of stringent glycemic control and targeted antifibrotic strategies to mitigate progression.

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