Abstract

ANIMAL MODELS OF NON-ALCOHOLIC FATTY LIVER DISEASES (NAFLD)

Amandeep Kaur, Shilpa Thakur, Amanpreet Kaur* and Dr. Naresh Singh Gill

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Abstract

Animal models play a crucial role in understanding the pathogenesis and therapeutic interventions of Non-Alcoholic Fatty Liver Disease (NAFLD). Dietary models, including High Fat Diet (HFD), High Fructose Diet, Methionine and Choline Diet (MCD), Atherogenic Diet, High Fat High Cholesterol Diet (HFHC), High Fat High Fructose Diet (HFHF), and Choline Deficient L-Amino-Defined Diet (CDAA), mimic human dietary patterns and induce NAFLD phenotypes in rodents. These models replicate various aspects of NAFLD, such as hepatic steatosis, inflammation, and fibrosis, by altering lipid metabolism, insulin sensitivity, and oxidative stress. HFD and high fructose diets induce hepatic lipid accumulation, resembling the metabolic abnormalities observed in human NAFLD. MCD diet, deficient in methionine and choline, leads to severe steatohepatitis and fibrosis. Atherogenic diets rich in cholesterol and cholate promote hepatic inflammation and atherosclerosis, representing NAFLD with cardiovascular comorbidities. HFHC and HFHF diets exacerbate hepatic steatosis and dyslipidemia, mirroring the effects of Western diets. Chemical models, like CDAA, induce liver injury by depleting essential nutrients, leading to hepatocellular damage and fibrosis. These models facilitate the study of NAFLD progression and the evaluation of therapeutic interventions. Overall, animal models of NAFLD, both dietary and chemical, provide valuable tools for investigating the underlying mechanisms of the disease, identifying potential therapeutic targets, and testing novel treatment strategies. These models contribute significantly to advancing our understanding of NAFLD pathogenesis and guiding the development of effective clinical interventions.

Keywords: Animal models, HFD, MCD, HFHC, HFHF, CDAA.