ATHENS, Ga. -- A team of researchers at the University of Georgia arethe first to determine that the hormone leptin causes the programmed death offat cells rather than simply reducing them in size.
Their discovery helps explain why rats injected with leptin stay thinlong after treatment has stopped, and could play a significant role in the useof leptin for the treatment of obesity, according to Clifton A. Baile,distinguished professor of foods and nutrition and animal science at UGA.
Research on leptin has exploded in the two years since it was firstdiscovered by Rockefeller University researchers. The hormone is produced by thebody's fat cells and travels through the blood stream to the brain. Animalstreated with leptin eat less, lose weight and expend energy at a higher rate.
Pharmaceutical companies have invested hundreds of millions in researchon the use of leptin to treat obesity and it's expected that leptin-basedmedication will be available within five years.
The UGA team's findings about leptin's effect on fat cells began afterthe arrival of Dr. Hao Qian (pronounced Hall Chin), a post-doctoral fellow whojoined UGA a year ago after spending several months researching apoptosis --programmed death -- of cells in the spinal cord following spinal-cord injuries.
In general, apoptosis is a routine process that occurs in most tissues.It is what causes leaves to fall from the trees in autumn and how the bodyeliminates diseased or unnecessary cells, such as a mother's milk-secretingmammary cells after a baby is weaned.
Apoptosis was first introduced in the scientific literature in 1972;however, extensive research on the role it plays in a variety of organismsdidn't begin until 1992, which explains why Qian's hypothesis about leptin'srole in the destruction of fat cells was so novel.
"When Hao first suggested that the fat cells' reaction to leptin lookedlike apoptosis, we didn't think he was right," Baile said. However, the teamdeveloped a series of experiments to test the hypothesis.
In their research, the UGA scientists injected one group of rats withleptin, a second group was placed on a low-calorie diet, while a third was givennormal amounts of food and not treated with leptin.
In comparing the DNA of the fat cells of rats treated with leptin andthe control groups, the fat cells of the leptin-treated rats clearly showedapoptosis. The DNA of the rats on the low-calorie diet and the control groupfailed to show any signs of apoptosis.
"The only cells affected in the leptin-treated rats were the fat cells,"Baile said. "Cells in the liver, kidney and heart, as well as both smooth andskeletal muscle were not affected. This was true in male and female rats, youngrats and older rats.
"A problem with most treatments for obesity is that once the treatmentis stopped, the individual begins gaining weight almost immediately," Baileexplained. "However, with leptin, that's not the case."
Baile said it takes weeks for the leptin-treated rats to recover the fatthey lose.
"We have had trouble finding any fat cells in rats within five days oftreatment," he said.
The scientists will present their results Oct. 27-28 in San Diego at theAnnual Conference on Apoptosis. Some of the research also was presented at aSeptember workshop sponsored by the National Institutes of Health that focusedon the brain and fat cells.
The above post is reprinted from materials provided by University of Georgia. Note: Materials may be edited for content and length.
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