Skip to main content icon/video/no-internet

Animal Models of Obesity

Complex physiological and behavioral conditions that occur in humans can be investigated in animal species that display, whether spontaneously or as a result of intervention, similar features of critical aspects of the condition being studied; such animals provide what is known as an animal model of the condition. In the case of obesity, the critical aspect is accumulation of excess body fat. Like humans, adequately nourished nonhuman species store body fat in amounts that support growth and reproduction; the percent of body weight that is due to fat at a given age may be quite consistent for the species despite variation in environmental conditions. However, like humans, other animal species can accumulate additional body fat (i.e., show an obese phenotype); this excessive accumulation may be associated with the behavioral and metabolic changes characteristic of human obesity.

Animal models can provide valuable information about human conditions that would be difficult or even impossible to obtain from human subjects. The shorter gestation periods and life spans of rodents, for example, make it possible to examine progression of obesity throughout life, as well as maternal effects on offspring and trends over many generations. Conditions in the animal's life, such as the composition and amount of food eaten, can be controlled and measured continually. Animal models make it possible, for example, to obtain tissues for study outside of the body, to use radioactivity or substances considered dangerous, to do surgery, or to implant devices in the brain, all of which can provide information crucial to understanding the condition in question. Perhaps the most exciting new use of animal models allows manipulation of the genome (the total deoxyribonucleic acid [DNA] of the organism) to uncover the roles that inherited traits play in controlling body fat accumulation and in mediating its effects.

Genetic Models

Animals living under standard conditions have been observed to spontaneously develop obesity; when this trait can be predictably passed to later generations, a genetic model of obesity may be defined. An example of a single-gene mutation that produces obesity is the ob/ob mouse. The recessive allele ob fails to produce the protein leptin, which the dominant allele Ob codes for; inheritance of both recessive alleles leads to absence of leptin and extreme obesity. Study of this genetic model led to the discovery of the hormone leptin, synthesized in adipose tissue, which inhibits feeding, increases energy expenditure, and alters metabolic pathways such as fat oxidation. Other spontaneous single-gene mutations have been shown to produce obesity in animal models; combinations of several genetic traits (polygenic models) may also be responsible for inherited obesity.

The genome can be manipulated in the animal to prevent the production of the protein coded for by a particular gene; this technique produces a genetic knockout model for the particular trait. The opposite effect, overexpression of a particular gene, can also be produced. These effects are bodywide unless techniques are used to produce tissue-specific effects. For example, nonfunctional membrane receptors for insulin might be produced only in certain tissues but not others; this would assist in the study of insulin resistance (a condition in which insulin is ineffective in producing its effects on cells), one of the metabolic effects of obesity. New traits can be introduced into the genome as well, utilizing viruses to carry the genetic information to targeted cell types. An example is introduction of a functional leptin gene (Ob) into specific tissues of an ob/ob mouse.

...

  • Loading...
locked icon

Sign in to access this content

Get a 30 day FREE TRIAL

  • Watch videos from a variety of sources bringing classroom topics to life
  • Read modern, diverse business cases
  • Explore hundreds of books and reference titles

Sage Recommends

We found other relevant content for you on other Sage platforms.

Loading