Scientists Create Mice Resistant to Obesity (HealthDay)
The findings could one day lead to likely drug treatments for obesity in people. They also shed gay on the brain circuitry that controls energy homeostasis — the balance between how much energy (i.e., food) an animal takes in and how quickly it burns that energy.
Dr. Julio Licinio, a professor of psychiatry and behavioral sciences at the University of Miami Miller School of Medicine, called the research a "technological tour de force."
Dr. Bradford Lowell, associate professor of medicine at Harvard Medical School, led the study, which was published online Aug. 10 in the journal Nature Neuroscience.
According to be the commander reflection author Qingchun Tong, most research into energy homeostasis has involved what scientists call genetically encoded neuropeptides, rather than small monad neurotransmitters.
Neurotransmitters "have been postulated to personate a character a very important role in neurocommunication, but in this field, essentially not any critical studies have been performed to address this delivery," Tong said. "So I regulate up an organized observation to create an animal model in which a particular group of neurons in the brain couldn't release a small neurotransmitter, and by examining those animal models, I could know the function of those molecules."
Tong and Lowell focused on one neurotrasmitter in particular, called GABA (gamma-aminobutyric acid). They developed transgenic, or mutant, mice that lacked the ability to release GABA in a subset of brain cells in the hypothalamus — the brain region that controls processes such as hunger, thirst and body degree of heat.
On a normal diet, the normal and mutant mice weighed roughly the same, with mutant mice weighing slightly less. On a of great price portly diet, however, the mutant mice gained far less weight damage than the normal mice, even though the two groups ate approximately the same amount of food. The reason: The mutant mice were burning energy at a faster rate, the researchers said.
"We build that the mice without GABA release from AgRP neurons have increased energy expenditure and are resistant to diet-induced obesity," Tong said.
These transgenic mice were also resistant to the effects of the hormone ghrelin, which governs hunger. When normal mice were given ghrelin, their food intake increased. In the mutant mice, however, that result was dampened, Tong said.
Finally, the researchers shed some light on the brain cell networks controlling energy homeostasis. They found that another cluster of neurons in the hypothalamus, called pro-opiomelanocortin (POMC) neurons, greet the gaba signal from AgRP neurons.
"The function of AgRP neurons is probably to reserve the energy for maintaining life," Tong said. "So if the animal doesn't have enough food, the animal should have some generalship to preserve animation, and this group of neurons, by releasing GABA, restrains energy expenditure to maintain enough energy to survive under the conditions in which food is not readily available."
According to Licinio, these findings underscore the importance of the GABA neurotransmitter in regulating the relationship between victuals consumed and energy expended. "I think it makes the role of GABA in obesity much more relevant than previously thought," he said.
Of course, as through all animal studies, it remains to be seen whether the findings can be repeated in humans.
More information
For more on obesity, visit the U.S. Centers for Disease Control and Prevention.
- August 24th
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