In the United States, more than 60 million adults are obese, meaning they are 20 per cent or more above the ideal weight for a person's height. Complications from obesity can include heart disease, diabetes and high blood pressure. Obesity results from environmental and lifestyle factors, which can be controllable, and from physiological factors, for which there is no conscious control. The physiological factors are genetically regulated.
A genetic link to obesity was strongly inferred by the results of studies involving twins who were raised apart. The study allowed the influences of genetic make-up and environment to be distinguished. These studies determined that genetic factors contribute to about 40 per cent of obesity variance in twins. Although genetic factors alone can not explain the large increase in the prevalence of childhood and adolescent obesity, interactions between genetics and environmental factors are likely. A person with a genetic disposition towards obseity, raised in an environment where consumption of high-fat food and little exercise are the norms, is likely to become obese. Susceptibility to obesity is largely a function of genetics, but the environment determines phenotypic expression.
Research into obesity has also utilized genetically engineered strains of mice. In 1997, researchers identified a gene in obesity-resisting mice called UCP2. The gene product may act to raise the body temperature, necessitating an increased use of calories. Conversely, malfunctioning UCP2 may increase the likelihood of fat accumulation, as the requirement for the expenditure of calories is less.
Five mouse strains currently exist for which obesity is a phenotypic trait. Research on these strains has identified a gene designated as ob (for obese). The ob gene product is a protein called leptin. The gene has been designated LEP. Leptin acts on the hypothalamus, a portion of the brain that regulates body functions. If a large amount of leptin is produced, the hypothalamus reacts by reducing appetite and accelerating the body's metabolism. But if the ob gene is defective and the amount of leptin is reduced, the hypothalamus might be induced to continually signal a need for food.
LEP and four other genes have been implicated in human obesity: PCSK1, LEPR, POMC and MC4R. Other genes, which have been associated or linked with human obesity phenotypes now number above 200. The genetic link to obesity may be an evolutionary holdover. Primordial ancestors existed in a harsh environment in which subsistence depended on hunting and gathering. Physical activity was mandatory for survival and periodic famine was the norm. Today's environment is often one of plentiful, easily obtainable food. Because the gene pool has not changed substantially, the genes, which favored survival now, favor obesity.
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