IN-VIVO MODELS OF NON-ALCOHOLIC FATTY LIVER DISEASE

Non-alcoholic fatty liver disease (NAFLD), a common chronic liver condition, is high in developed nations. One of the factors leading to chronic liver disease and cryptogenic cirrhosis has been identified as NAFLD. Multiple risk factors, including obesity, insulin resistance, diabetes mellitus, hyperlipidemia, and hypertension-related cardiovascular disease, contribute to the development of NAFLD. The pathogenesis of NAFLD involves a complex interplay among several key pathological processes, including insulin resistance, abnormal lipid metabolism, oxidative stress, inflammation, apoptosis, and fibrosis. The initial stage of NAFLD, known as hepatic steatosis, manifests as excessive fat accumulation within the liver. Although extensive research efforts have led to the identification of these risk factors, there remains a limited understanding of the disease initiation and the underlying molecular mechanisms driving its progression. Animal models of NAFLD give crucial information, not only in elucidating the pathogenesis of NAFLD but also in examining the therapeutic effects of various agents. An ideal model of NAFLD should correctly reflect both hepatic histopathology and the pathophysiology of human NAFLD. This review summarizes diet-induced and genetic animal models, used in recent years to add to the understanding of the mechanisms involved in NAFLD.