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T he field of genetics has evolved rapidly since 2000. New technology has allowed researchers to identify genes, which provide the blueprint necessary for the body to manufacture specific hormones like insulin and estrogen. These hormones tell the body to store or burn fat, carbohydrates, and protein. Additionally, hormones maintain body temperature, regulate digestive rate, tell the body to stop or start eating, and initiate growth in children and adolescents. When a person does not have a gene that is essential for the production or activation of a hormone, a disease usually develops. For example, a person who lacks the gene to manufacture growth hormone (pituitin) will not be able to grow to normal height. People can carry a gene without having the disease, which means that a child can inherit a disease that neither parent has.

As scientists discovered genes that seemed to trigger diseases such as cancer and diabetes, they began searching for genes that cause weight gain or loss as well. Genes in animals are very similar to those in humans, thus animals are frequently used to find new genes and to understand their function. In the 1940s, a gene in mice was discovered that was the blueprint for a hormone called leptin (Kalra et al. 2003). Leptin is secreted in response to the amount of fat in the body of the animal. The release of leptin decreases appetite and tells the mouse to stop eating. If the gene producing leptin is missing, the mouse will not stop eating and will gain significant amounts of body fat. When the animals are injected with leptin, they will stop eating and return to normal weight (Stipanuk 2000: 443-4).

The discovery of the function of leptin led researchers to predict that if leptin was administered to obese individuals, they would lose weight. Despite unsuccessful clinical trials, drug companies began to market leptin in the form of over-the-counter dieting supplements like Leptoprin. The problem with these supplements is that leptin is minimally effective in controlling weight when injected and completely ineffective when taken orally. As of 2007, leptin had not yet been shown to be a useful treatment for weight loss, but the research is still ongoing. A very few families have been identified who possess copies of the ob gene from both parents; their obesity was indeed treatable through the use of leptin (Small and Bloom 2004: 117).

Although leptin was not the answer to weight loss that scientists had hoped, research to locate a gene responsible for fat gain continued. As with leptin, if a hormone could be discovered that reduces body weight, the pharmaceutical industry could potentially manufacture and distribute the hormone as a drug or supplement to aid in weight loss. Two hormones of interest are ghrelin (Small and Bloom 2004), discovered in 1996, and obestatin (Zhang et al. 2005), discovered in 2005. The role of ghrelin in obesity is not fully understood, yet obese individuals tend to have lower levels of this hormone compared with nonobese people. Additionally, people suffering from anorexia nervosa tend to have higher ghre-lin levels than people of normal weight (Gale et al. 2004). These two findings have led researchers to believe that ghrelin is an important hormone for controlling appetite. Obestatin decreases the appetite of mice and could possibly do the same in humans (Zhang et al. 2005).

There are also pathological explanations for the inheritance of obesity. There are over forty different complex syndromes listed in the on-line "Mendelian Inheritance in Man" database that include "obesity" as one of their diagnostic criteria. Yet each may well be triggered by different combinations of genes for different reasons (Bray and Allison 2001: 9). The discovery of these and other hormones could provide a scientific basis to treat individuals who have high body fat in the same way that doctors treat high blood pressure or cholesterol (Scharf and Ahima 2004; Orr and Davy 2005). Furthermore, such genetic anomalies could also be detected by genetic screening in analogy to Downs Syndrome and identify high-risk individuals.

SLG/Suzanne Judd

References and Further Reading

Syndromes," in John B. Owen, Janet Treasure, and David A. Collier (eds), Animal Models: Disorders of Eating Behavior and Body Composition, Dordrecht: Kluwer, pp. 1-18.

Gale, S.M., Castracane, V.D. and Mantzoros, C.S. (2004) "Energy Homeostasis, Obesity and Eating Disorders: Recent Advances in Endocrinology," Journal of Nutrition 134 (2): 295-8.

Kalra, S.P., Bagnasco, M., Otukonyong, E.E., Dube, M.G. and Kalra, P.S. (2003) "Rhythmic, Reciprocal Ghrelin and Leptin Signaling: New Insight in the Development of Obesity," Regulatory Peptides 111 (1): 1-11.

Orr, J. and Davy, B. (2005) "Dietary Influences on Peripheral Hormones Regulating Energy Intake: Potential Applications for Weight Management," Journal of the American Dietetic Association 105 (7):


Scharf, M.T. and Ahima, R.S. (2004) "Gut Peptides and Other Regulators in Obesity," Seminars in Liver Disease 24 (4): 335-47.

Shell, Ellen Ruppel (2001) The Hungry Gene: The Science of Fat and the Future of Thin, New York: Atlantic Monthly Press.

Small, C.J. and Bloom, S.R. (2004) "Gut Hormones and the Control of Appetite," Trends in Endocrinology and Metabolism 15 (5): 259-63.

Stipanuk, M.H. (2000) Biochemical and Physiological Aspects of Human Nutrition, Philadelphia, Pa.: Saunders.

Zhang, J.V., Ren, P.-G., Avsian-Kretchmer, O., Luo, C.-W., Rauch, R., Klein, C. and Hsueh, A. (2005) "Obestatin, a Peptide Encoded by the Ghrelin Gene, Opposes Ghrelin's Effects on Food Intake," Science 310 (5750): 996-9.

See also Anorexia; Friedman; Hormones Used in Dieting

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