Gerbils (Meriones unguiculatus) as a new experimental model of obesity induced by diet

Background. Currently, the number of obese people in the world has reached alarming proportions. During the expansion of adipose tissue, a number of functions such as activation and release of cytokines and hormones may be affected. This causes the body to take a proinflammatory pattern, which may affect the proper functioning of many tissues. Thus, studying the mechanisms by which obesity induces physiological disorders is necessary, and may be facilitated by the use of animal models, in particular rodents. We sought to investigate whether the gerbil (Meriones unguiculatus) would be a good experimental model for the study of obesity and metabolic changes resulting from a diet rich in fats and sugars. Methods. 14 gerbils were divided according to weight into two experimental groups and received a a standard diet with 4,15kcal/g (CT; n = 7) or a diet rich in simple carbohydrates and fats with 5,86kcal/g (OB, n = 7) for 11 weeks. The animals had free access to water and food. The weight of each animal and food consumption of each cage were measured weekly and at the end of the experiment, blood, adipose tissue and liver were collected. The following parameters were determined: cholesterol (COL), triglycerides (TGL) and glycemia (GLI) in the plasma; cytokines (IL-6, IL-10 and TNF-α) and hormones (adiponectin and leptin) in adipose tissue; activity of superoxide dismutase (SOD) and catalase (CAT), extraction and differentiation of fat in the liver and liver histology. Results. The consumption of a diet rich in simple fats and carbohydrates led to an increase of total body weight, relative weights of liver and adipose tissue, glucose and triglycerides levels, and TNF-α concentration in adipose tissue. Animals of this group also showed a significant increase of total fat, cholesterol and triglyceride content in the liver, contributing to higher intensity of hepatic steatosis. On the other hand, depletion in the enzyme activity of SOD and CAT in the liver, as well as reduction of IL-10 and adiponectin levels were found in adipose tissue of these animals. Conclusion. Diet consumption consisting of an excess in saturated fat and simple carbohydrates establish the gerbil as an experimental model for the study of obesity and metabolic and liver abnormalities resulting from this disease. 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 PeerJ Preprints | https://doi.org/10.7287/peerj.preprints. 2535v1 | CC BY 4.0 Open Access | rec: 17 Oct 2016, publ: 17 Oct 2016 Introduction In past decades, malnutrition was the main nutritional disorder requiring multi-professional care. Currently, much of the world's population has experienced the opposite problem, and the number of obese people in the world, has reached alarming proportions. The change in dietary pattern of the world population, making it rich in calories from fats and sugars, associated with physical inactivity, significantly increased prevalence of obesity not only in developed countries but also in developing ones (WHO, 2016). This fact has drawn much attention since obesity is strongly associated with increased risk of developing metabolic syndrome, characterized by central obesity, insulin resistance, dyslipidemia, increased blood pressure and nonalcoholic fatty liver disease (NAFLD) (Lumeng & Saltiel, 2011). Adipose tissue is not simply an energy inert deposit, but is a multifunctional organ, that exerts important endocrine and immune functions (Lumeng & Saltiel, 2011; Clemente-Postigo et al, 2011; Gregor & Hotamisligil, 2011). Adipocytes are mainly responsible for the activation and release of substances, such as cytokines IL-6, TNF-α and hormones such as leptin and adiponectin (Trujillo et al, 2004; Jung & Choi, 2014). During the expansion of adipose tissue, these functions may be affected, leading the body to a pro-inflammatory pattern, which may affect the proper functioning of many tissues (Wellen & Hotamisligil, 2005). It is believed that the inflammation induced by obesity contributes to the development of many chronic diseases, including type 2 diabetes mellitus, atherosclerosis, liver disease and some forms of cancer (Lumeng & Saltiel, 2011; Gregor & Hotamisligil, 2011; Jung & Choi, 2014). The study of the mechanisms by which obesity induces physiological disorders may be facilitated by the use of animal models, in particular rodents (Panchal and Brown, 2011; Nilsson et al, 2012). Considering that, despite its etiology, the number of obese individuals in the world is increasing, it is suggested that environmental or behavioral factors, such as food, are the main contributors to the epidemic, rather than genetic changes (Buettner, Scholmerich & Bollheimer, 2007). Thus, whereas the experimental model should be as close as possible to the genesis of study, polygenetic animal models with diet-induced obesity have been preferably used in place of monogenetic models (Rosini, Silva & Moraes, 2012). Due to their size, ease of handling, and similarity to patterns found in humans (Eckmann, 2003; Araújo et al, 2008), the gerbil (Meriones unguiculatus) is a model already widespread in many 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73