Obesity is one of the major risk factors for the Nonalcoholic Fatty Liver Disease (NAFLD) development, as the leading cause of chronic liver disease. NAFLD is intrinsically related to obesity disorders, especially insulin resistance and dyslipidemia. Interaction between NAFLD and obesity still needs further clarification, and it is necessary to dertemine the mechanisms of these disorders in animal models of disease. Such models are usually the result of genetic and/or nutritional modifications, considering metabolic and histological changes commonly seen in humans. Obesity induced in rodents occur mainly through HFD, HCD, FFD or genetic alterations like in Lep, Acox, KKy models. These models are analogous to NAFLD development, since the increasing visceral fat is highly associated with the accumulation of fat in the form of triglycerides in the liver. Inflammatory markers such as TNF-alpha and IR are active in the predisposition of lipolysis. Hepatic inflammation during NAFLD can also be unleashed by oxidative stress. However, the mechanisms involved in the progression from NAFLD to NASH are not yet elucidated, as some models have shown unexpected outcomes such as severe malnutrition or obesity markers absence and IR after the use of Minimal-change disease (MCD) therapies and drugs, respectively. Thus, it is important to evaluate different animal models of obesity able to induce the profile of NAFLD and NASH disease in humans, assessing their mechanisms of action. The aim of this chapter is to have a comparative analysis of animal models commongly used in the pathophysiology of obesity that present NAFLD/NASH.
Part of the book: Experimental Animal Models of Human Diseases