Chapters authored
Animal Models of Obesity Characterized by Non-alcoholic Fatty Liver Disease (NAFLD)
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
Use of Animal Models in the Study of Colitis
Inflammatory bowel diseases (IBDs) relate to chronic inflammations in different parts of the gastrointestinal (GI) tract involving both ulcerative colitis (UC) and Crohn’s disease (CD). Ulcerative colitis begins in the rectum and extends continuously up the colon. Notably, CD may affect any area of the GIT, from the mouth to the anus. Various conditions may influence the genesis of the disease, such as genetics, environment, intestinal microbiota and the presence of agents of enteric infections. Experimental models are therefore suitably used to investigate the various etiological factors; similarly colitis can be induced by genetic modification, cell transfer, spontaneous inflammation and chemical agents. The objective of this chapter is to present current concept on animal models of inflammatory bowel diseases. These models are crucial for the understanding of inflammatory bowel diseases, development of alternative treatments and more effective therapeutic agents thus contributing to the control of the disease.
Part of the book: Experimental Animal Models of Human Diseases