Single Gene Could Play Role in Obesity
(Ivanhoe Newswire)– A ravenous appetite may be what causes many overweight people to be obese. Researchers have found a mutation in a single gene is responsible for the inability of neurons to effectively send out appetite suppressing signals from the body to the correct area of the brain.
A study suggests that there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating.
Researchers found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to adequately pass leptin and insulin chemical signals through the brain. In humans, these hormones are designed to “tell” the body to stop eating. But if the signals fail to reach correct locations in the hypothalamus, the area in the brain that signals satiety, eating continues.
“This is the first time protein synthesis in dendrites, tree-like extensions of neurons, has been found to be critical for control of weight,” Baoji Xu, Ph.D., study’s senior investigator, an associate professor of pharmacology and physiology at Georgetown, was quoted as saying.
“This discovery may open up novel strategies to help the brain control body weight,” he said.
Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons.
Xu also found that the mice with the same Bdnf mutation grew to be severely obese.
Other researchers began to look at the Bdnf gene in humans, and large-scale genome-wide association studies showed Bdnf gene variants are, were also linked to obesity.
However, until this study, no one has been able to describe exactly how BDNF controls body weight.
Xu’s data shows that both leptin and insulin stimulate synthesis of BDNF in neuronal dendrites in order to move their chemical message from one neuron to another through synapses. The intent is to keep the leptin and insulin chemical signals moving along the neuronal pathway to the correct brain locations, where the hormones will turn on a program that suppresses appetite.
“If there is a problem with the Bdnf gene, neurons can’t talk to each other and the leptin and insulin signals are ineffective, and appetite is not modified,” Xu said.
“We have opened the door to both new avenues in basic research and clinical therapies, which is very exciting” Xu was quoted as saying.
SOURCE: Nature Medicine’s, March 2012