About two-thirds of American adults are overweight or obese, according to the National Institutes of Health. As obesity reaches epidemic portions, weight related disorders such as diabetes and heart disease are on the rise, threatening the health and well-being of more Americans and straining medical resources. Leptin, a hormone produced in fat cells, has gained the attention of researchers because of its role in regulating hunger, satiation, and energy use and storage.
Leptin
In the mid-90s, Jeffrey M. Friedman, M.D., Ph.D. described a gene in mice and humans, which he called the obese gene. This gene detected the presence of a hormone Friedman dubbed leptin, based on "leptos," the Greek word for thin. Leptin is a protein-based hormone released by fat cells that affects a variety of physiological and behavioral functions, including reproduction, immune function, metabolism and, perhaps, consumptive behavior. Friedman and others found that both mice and humans with more body fat have higher levels of leptin.
Normal Function
Leptin levels are determined by several factors, including your caloric intake, insulin levels and amount of body fat. If you are of normal weight, leptin provides a signal to the brain regarding the status of energy storage. After you've eaten, calories you don't use immediately are converted into fat for future use. As your stores of fat fill up, your fat cells release leptin into your bloodstream, distributing it to your brain and to tissues throughout your body. Leptin instructs your brain and body that you have plenty of energy stored. Leptin decreases hunger and signals your body to start burning calories, because your stores are full and you don't need to obtain or conserve energy.
Elevated Leptin in Obesity
People who are obese have more fat and consequently have greater amounts of leptin. Ordinarily, the increased level of leptin should signal the brain that energy stores are full and should decrease hunger and stop eating behavior. However, the persistent pattern of excessive eating and elevated leptin associated with obesity creates a condition called leptin resistance; those with excessive fat tissue no longer respond to the release of leptin. Circulating leptin, whether released by their own fat tissue or administered orally, fails to curb appetite and fails to enhance metabolism to burn more fat. Once leptin resistance develops, it leads to a cycle of escalating accumulation of fat. Also, though it doesn't curb appetite or trigger the use of energy, the increased release of leptin in obese people has adverse effects, such as promoting inflammation, according to "The (reference: International Journal of Obesity and Related Metabolic Disorders."
Causes of Leptin Resistance
Leptin resistance is linked to obesity, but certain types of diets also seem to increase the risk for leptin resistance, such as diets high in fat, according to research reported in 2009 in "The American Journal of Physiology." Diets high in fructose, the sugar found naturally in fruit, do the same. Animal evidence suggests that leptin resistance increases with age, because aging causes a decrease in the number of leptin receptors in your brain.
Reducing Leptin Resistance
When working properly, leptin helps your body manage energy. When fat stores get low, your metabolism slows down to conserve energy use. Modern societies provide plentiful high-calorie, high-fat foods, a condition that seems to disrupt the normal feedback pathways that regulate your body's energy use. To restore the normal cycle, reduce your consumption of sweetened and high-fat food. Reduce your overall caloric intake so you lose weight and body fat. And exercise daily to use up fat stores and aid weight loss.
References
- "American Journal of Physiology": Leptin Resistance
- "Journal of Endocrinology": Decreased Leptin Uptake in Hypothalamic Nuclei
- National Institutes of Health: Weight Control
- Obesity: Leptin Resistance and Obesity
- Proceedings of the National Academy of Sciences: Circumventing Leptin Resistance for Weight Control
Member Comments