2004 Obesity Lecture 4




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Summary: By four years old, the boy weighed 90 pounds and consumed more than 1,100 calories in a single sitting-approximately half the recommended daily intake for an adult. Genetic testing revealed that the child possessed a rare mutation that disabled his leptin gene. Without the hormone, he kept gaining weight because his body told his brain that he was starving. When doctors treated the boy with leptin, his calorie intake was slashed by 84 percent and he eventually got down to a normal weight for his age. In studies of obese mice, Dr. Friedman has found that leptin actually restructures the brain, rewiring the neural circuit that controls feeding. The hormone reinforces the nerve cells that encourage the body to slenderize and prunes the neurons that compel eating. Leptin isn't the whole story. For most of us, a combination of genes regulates our weight. These powerful systems are part of our genetic heritage. Some researchers think that such "thrifty genes" provided our ancestors with a survival strategy for coping with famine. Individuals who stored calories in times of plenty could avoid starvation when food grew scarce. Thus, obesity could be a product of these genes that evolved to keep us alive. Dr. Friedman describes his continuing hunt for the genes that make us fat, research that has carried him to a small island in the Pacific where obesity is rampant. By analyzing DNA collected from all the adults on the island, Dr. Friedman hopes to learn more about why some people are overweight while others are lean.