Diet-induced obese

The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets. It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models. These animals can then be used to study in vivo obesity, obesity's comorbidities, and other related diseases. Users of such models must take into account the duration and type of diet (e.g. hydrated gels vs. dry pellets) as well as the environmental conditions and age of the animals, as each may promote different bodyweights, fat percentages, or behaviors. The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets. It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models. These animals can then be used to study in vivo obesity, obesity's comorbidities, and other related diseases. Users of such models must take into account the duration and type of diet (e.g. hydrated gels vs. dry pellets) as well as the environmental conditions and age of the animals, as each may promote different bodyweights, fat percentages, or behaviors. Driven by the worldwide epidemic of obesity, particularly in the Western world, the DIO model has been integral in understanding the relationship between high-fat/high-density diets and obesity, including the discovery of Akt and mTOR, signals in the body linked to obesity and insulin resistance. However, while many insights into the control of obesity have come from experiments since its introduction in 1949, the use of animal models does restrict our ability to extrapolate findings to humans. The DIO model was developed in response to growing concerns over the health effects of obesity, as well as the rapid growth of the obesity rate in countries around the world. As such, the model was developed in order to create a controlled environment for the study of how obesity develops, as well as its effects. The model was used as early as 1949, and has expanded far and wide in its use and goals. Social and environmental determinants may also induce the onset of obesity. Social class may affect individual access to proper nutritional education and may hinder an individual's ability to make healthy lifestyle choices. Additionally, samples of low-income women and children were also shown to have higher rates of obesity because of stress. Exposure to pollutants such as smoke and second-hand smoke have also shown direct correlations to obesity. Studies on the relationship between infectious agents and weight gain show that certain species of gut flora can affect metabolic processes. This correlation links these gut bacteria to an inability to digest complex polysaccharides. Certain viruses, specifically the AD-36 adenovirus, have been shown to increase body fat in laboratory animals. Living a sedentary lifestyle is one of the leading factors in causing obesity. As of 2016, over 30% of people in the world don't get enough exercise. Genetic mutations to genes monitoring metabolism and appetite predispose people to obesity. Various syndromes resulting in genetic polymorphisms lead to obesity. A few common examples are: Prader-Willi syndrome, Bardet-Biedl syndrome, Cohen syndrome, and MOMO syndrome. Multiple mental and physical illnesses, along with some of the medications that treat such illnesses can increase someone's risk of obesity. Some examples of other illnesses are hypothyroidism, Cushing's syndrome, and growth hormone deficiency. Obesity is affected by 'environmental, biological, and psychosocial pressures', therefore it is understandable that several limitations are established when translating results between the results of a diet induced obesity model in a lab and humans. While models are an important method of investigating the influences of obesity and drug testing, it is important to understand the limits of the model's overall ability to resemble the human obesogenic pathophysiology. Such limitations can be divided into three broad categories—biological, dietary and experimental differences—factors including, but not limited to, the genetic makeup of the species or strain, the environment in which the specimen is held (temperature, light, number of animals), age, sex, the duration of the experiment, and the texture or type of rations fed to the animals.