Obese Mouse Model, Animal Models of Obesity

Animal Model Obesity

Obesity is a combination of genetic factors and environmental factors caused by nutritional metabolic disorders. Prevention and treatment of obesity has become an important health problem in the 21st century. Animal models are an essential for the study of obesity.

Animal modeling is extremely critical for early work for obesity research. Only successful animal model of obesity can be used to study the mechanism of obesity and its treatment. Here are two ways that will be mentioned: Food-induced obese animal models and glutamate – induced obese animal model.

Food ingredients and energy are currently the source of obesity epidemic and different types of food can replicate obese animal models. The essential condition for replicating an obese animal model is to provide a hot card that must exceed the amount of heat required by the body.  Mercer and so on to compare the effects of three different feed configurations on the rat’s bait obesity, from normal feed to high energy HE pellet feed; high energy feed and then add complete liquid feed EN; remove HE or HE + EN back to ordinary pellet feed the results showed that SD rats from general diet to HE diet could be divided into two groups: obesity susceptibility and obesity resistance.

Rats with the highest weight gain or the lowest weight gain after 40 weeks of feeding HE diet were divided into susceptible group and the resistance group, the susceptible group continued to feed the HE diet, the supplement group added the chocolate flavor liquid feed EN, the resistance group supplemented with EN can cause additional weight gain, after the activation was sustained super-calorie consumption, of the susceptible group of similar weight, then the two groups returned to feed the feed, the previous fed HE group continued to maintain elevated body weight, can effectively maintain body weight stability. While the resistance group at the same time evacuation of HE and EN caused by energy intake and weight loss.

The above results suggest that high energy feed is essential to induce obesity. Liu Qingchun selected improved formula also successfully caused the rat model of nutritional obesity. Zhang Tao and other self-made high-fat high-energy feed to establish SD rat obese animal model. The formula reduces fat and salt content and adds TC and PTU. It is believed that the adjusted formula is not only beneficial to the molding and feed utilization in feed processing, but also the addition of TC and PTU feed is theoretically more favorable for obese animal model preparation. Shen Ruling also used high fat diet method successfully caused large, mouse obesity model.

Subcutaneous injection of MSG in neonatal mice or rats can induce it to produce obesity. The detailed mechanism of MSG animal obesity is unclear. MSG caused by obesity is due to nodular funnel dopamine system damage caused by endocrine and other dysfunction caused by metabolic disorders caused. The method of modeling generally occurs after 6 weeks of progressive obesity, 4 to 5 months of age when the weight gain tends to be stable. This obese animal is mainly due to fat accumulation, the body short to Lee’s index significantly increased with no significant increase in body weight, food intake does not increase, and there is a tendency to reduce. Its activities to reduce the ability to learn differences weakened.

Therefore, from the appearance to determine whether the animal is obese, only from the body shape and Lee’s index to judge, rather than food intake and weight, generally do not use appetite suppressant drugs and the observation of the subject. The results showed that plasma TG, ALP, phospholipid, STB and its free fatty acids, VLDL, ALT, CHE, TC were increased; and phospholipid in the liver unchanged, VLDL increased, TG increased. Hormone-sensitive lipase digestibility was significantly reduced. Female animals also show ovarian, uterine weight loss, glucocorticoid levels increased. Detection of serum T3 and free thyroid hormone levels, found that hypothyroidism.

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