Acute, sub-chronic or chronic feeding studies can be performed in any commercially available genetically-obese rodent model, including:
Genetically obese animals are monogenic. This means the obesity has arisen from spontaneously occurring single gene mutations which prevent the production of the adipose hormone, leptin (ob/ob mice), or result in deficient leptin receptors (db/db mice and Zucker fatty fa/fa rats).
Genetically obese rats and mice have been well characterised and widely used in obesity research. However, it is now generally accepted that genetic models of obesity do not mimic human obesity as well as animals made obese by exposure to high fat or cafeteria diets. The main reason for this is that the genetic predisposition to obesity in most humans is polygenic in nature. Single gene mutations have been linked to obesity in man, but such instances are extremely rare.
Although studies in ob/ob mice, db/db mice and Zucker fatty fa/fa rats are no longer used as primary screens to measure the effects of drugs on body weight, they can still provide useful additional information regarding the antiobesity potential of novel compounds and their effects on diabetic endpoints.
Effect of rimonabant on body weight in male fa/fa zucker rats
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