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Researchers show how obesity causes breakdown in system which regulates appetite and weight
March 07, 2007PORTLAND, Ore. - New research led by scientists at the Oregon National Primate Research Center demonstrates how obesity causes the breakdown of a brain system that regulates appetite. The research provides a clear picture of some factors involved in obesity. More than 60 percent of American adults are overweight and more than 30 percent are obese The study results may have also identified possible targets for new drug therapies aimed at assisting individuals in weight loss. The research is published in the March issue of Cell Metabolism.
The research provides new understanding of leptin resistance. Leptin is a hormone secreted by fat cells. It can suppress food intake by affecting brain cells that control appetite. However, high levels of leptin which can be found in severely overweight individuals, can lead to leptin resistance. Leptin resistance means that the body no longer responds to the hormone's weight suppressing effects.
The research was conducted in mice and involved two separate groups that were fed high-fat and low-fat diets. Over time, the high-fat diet group developed symptoms of diabetes and obesity, as is often the case in humans. The low-fat diet group did not develop these health problems.
"This research demonstrates how a portion of the hypothalamus of the brain, called the arcuate nucleus, is negatively impacted by an overabundance of leptin," explained Michael Cowley, Ph.D., an associate scientist in the Division of Neuroscience at ONPRC. "By developing a special test of neuronal function, we were able to witness the breakdown in this group of specialized cells. Eventually the cells behaved as if there was no leptin present, even though levels were 40-times higher than in normal animals. We were also able to witness the eventual repair of this important system which occurs as the mice lost weight when returned to a low fat diet."
More specifically, the scientists determined that leptin resistance prevented the arcuate nucleus from taking part in an important signaling function that regulates appetite and body weight. Meanwhile, other portions of the weight regulation system remained intact and in fact became more responsive, thereby suggesting that arcuate nucleus function is the point of breakdown during leptin deficiency.
Finally the research highlighted a key gene called SOCS-3 involved in leptin deficiency. By targeting the gene with therapeutics, scientists may be able to repair leptin deficiency, aiding in weight loss.
"Of course these findings are quite far from the development of a weight loss drug," explained Cowley. "This work further highlights the essential role of SOCS-3 in this critical regulation system."
"One of the surprising things was when we put the genetically identical mice on the high fat diet, some became obese, and some did not. One major difference between these groups of mice was the activity of SOCS-3," said Pablo Enriori Ph.D. of Cowley's lab, first author of the paper. The research was conducted in conjunction with Brown University in Rhode Island.
Oregon Health & Science University
"This research demonstrates how a portion of the hypothalamus of the brain, called the arcuate nucleus, is negatively impacted by an overabundance of leptin," explained Michael Cowley, Ph.D., an associate scientist in the Division of Neuroscience at ONPRC. "By developing a special test of neuronal function, we were able to witness the breakdown in this group of specialized cells. Eventually the cells behaved as if there was no leptin present, even though levels were 40-times higher than in normal animals. We were also able to witness the eventual repair of this important system which occurs as the mice lost weight when returned to a low fat diet."
More specifically, the scientists determined that leptin resistance prevented the arcuate nucleus from taking part in an important signaling function that regulates appetite and body weight. Meanwhile, other portions of the weight regulation system remained intact and in fact became more responsive, thereby suggesting that arcuate nucleus function is the point of breakdown during leptin deficiency.
Finally the research highlighted a key gene called SOCS-3 involved in leptin deficiency. By targeting the gene with therapeutics, scientists may be able to repair leptin deficiency, aiding in weight loss.
"Of course these findings are quite far from the development of a weight loss drug," explained Cowley. "This work further highlights the essential role of SOCS-3 in this critical regulation system."
"One of the surprising things was when we put the genetically identical mice on the high fat diet, some became obese, and some did not. One major difference between these groups of mice was the activity of SOCS-3," said Pablo Enriori Ph.D. of Cowley's lab, first author of the paper. The research was conducted in conjunction with Brown University in Rhode Island.
Oregon Health & Science University
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