The genome of human beings and various animals contains an obese gene that codes for hormone called "leptin." This hormone, as it circulates in the body, consists of 146 amino acids and has a molecular weight of 16 kilodaltons, according to the Kenyon College Department of Biology. A proton weighs one dalton, so a leptin molecule weighs as much as 16,000 protons. Leptin theoretically plays a role in several physiological functions, especially body fat regulation.
The Basic Theory
When mutated obese genes of mice cannot produce leptin, the mice become fat. When these fat mice are treated with leptin, they become thin. The consequent leptin theory postulated that adipose (fat) cells produce leptins and release them into the bloodstream. The amount of leptin in the bloodstream tells the hypothalamus how many adipose cells are present in the body. If the bloodstream is deficient in leptin, the hypothalamus quickens the appetite, but if there is too much leptin, the hypothalamus fosters a feeling of satiety and increases energy expenditure. The result is a reduction in the number of adipose cells in the body, accompanied by a loss of weight.
Problems with the Theory
Treatment with leptin helps people whose obesity is due to mutated genes that cannot produce leptin, but this condition rarely occurs in human beings. Obese people with normal genes usually have high levels of leptin in the blood stream, but the high leptin level does not reduce the number of adipose cells. In addition, when Dr. Steven Heymsfield conducted a controlled experiment administering leptin to obese subjects, the patients did not lose much weight, according to Columbia University Medical Center.
Modifications of the Theory
The failure of high leptin levels to produce its expected effect in obese human beings has led to modifications of the basic theory. Obese human beings may develop a resistance to leptin, or leptin may not be able to enter their central nervous system cells of obese humans, or it might be difficult for leptin to bind to its receptor site, according to Davidson College. Some abandon the basic theory and assign a slightly different physiological role to leptin. They say that leptin acts as a thermostat to maintain a constant body weight. This would explain why many people do not gain weight even though they eat a lot. For this reason, when obese subjects lose weight and then receive enough leptin to maintain their former leptin levels, the patient does not regain the lost weight because the brain perceives that the leptin level is normal and does not take action to increase the number of adipose cells, according to the Columbia University Medical Center and Rice University.
Other Considerations
The basic leptin theory does not take into account the complexity of leptin’s physiological functions. Leptin activity is modified by interaction with other hormones. For example, a hormone called neuropeptide Y is antagonistic to the action of leptin, according to Rice University. High leptin levels result in low levels of insulin, and the presence of leptin in hemopoietic (blood-producing) cells results in enhanced production of regulatory proteins called cytokines, according to Frontiers in Bioscience. Leptin also plays a role in reproduction. It induces the release of certain sex hormones, such as luteinizing hormone. In addition, leptin levels rise during pregnancy, and pregnant women usually have a hearty appetite in spite of it, according to Rice University.
References
- Rice University: Leptin as Fat Organizer; Jaime Hennessey; 2003 (PDF)
- Columbia University Medical Center: The Latest Skinny on Leptin
- "Science Creative Quarterly"; Leptin -- A Piece of the Obesity Pie; Minh Liu; 2011
- Encyclopaedia Britannica: Leptin
- Davidson College: Leptin
- Colorado State University: Leptin
- Kenyon College Department of Biology: Leptin-E100, the Obese Protein
- "African Journal of Biotechnology"; Stutdy of Polymorphism of...; H.A. Abbasi, et al.; March 2011 (PDF)
- Frontiers in Bioscience: Leptin, a Multifunctional Protein
- "Journal of Endocrinology"; Definition and Characterization of...; B. Buettner, et al.; 2002 (PDF)
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