A single gene's effect on the brain can result in non-stop eating, research has shown.

Scientists believe the "gluttony gene" may be responsible for cases of obesity caused by out-of-control appetite.

The Bdnf gene variant was studied in mice. It was found to prevent brain neurons from transmitting signals that tell the body it has eaten enough.

"This discovery may open up novel strategies to help the brain control body weight," said lead researcher Dr Baoki Xu, from Georgetown University Medical Centre in the US.

Hunger and satiety, the sensation of "feeling full", are governed by a complex balance of hormonal and neuronal signals.

Two hormones in particular, leptin and insulin, released in the body after a meal play a key role.

Their chemical signals activate neurons in the hypothalamus region of the brain that trigger satiety. But if the connection is not made, the craving for food continues.

"Short" versions of the Bdnf gene block the leptin and insulin signals and prevent the "stop eating" message passing through the brain to the correct appetite-suppressing locations, say the scientists.

The research is reported online in the journal Nature Medicine.

Bdnf makes a protein that is synthesised in dendrites, the branch-like "fingers" that project from nerve cells. Dendrites carry the synapses that neurons use to communicate to each other.

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'Gluttony gene’ may be behind big appetites

A single gene's effect on the brain can result in non-stop eating, research has shown.

Scientists believe the "gluttony gene" may be responsible for cases of obesity caused by out-of-control appetite.

The Bdnf gene variant was studied in mice. It was found to prevent brain neurons from transmitting signals that tell the body it has eaten enough.

"This discovery may open up novel strategies to help the brain control body weight," said lead researcher Dr Baoki Xu, from Georgetown University Medical Centre in the United States.

Hunger and satiety, the sensation of "feeling full", are governed by a complex balance of hormonal and neuronal signals.

Two hormones in particular, leptin and insulin, released in the body after a meal play a key role.

Their chemical signals activate neurons in the hypothalamus region of the brain that trigger satiety. But if the connection is not made, the craving for food continues.

"Short" versions of the Bdnf gene block the leptin and insulin signals and prevent the "stop eating" message passing through the brain to the correct appetite-suppressing locations, say the scientists.

The research is reported in the journal Nature Medicine.

Bdnf makes a protein that is synthesised in dendrites, the branch-like "fingers" that project from nerve cells. Dendrites carry the synapses that neurons use to communicate to each other.

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'Gluttony gene' may explain out-of-control appetite

London, March 19 (ANI): Researchers have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain, which results in obesity caused by a voracious appetite.

Researchers at Georgetown University Medical Center suggested there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating.

The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain.

In humans, these hormones, which are released in the body after a person eats, 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," said the study's senior investigator, Baoji Xu, Ph.D., an associate professor of pharmacology and physiology at Georgetown.

"This discovery may open up novel strategies to help the brain control body weight," he noted.

Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons.

For example, he has shown that during development, BDNF is important to the formation and maturation of synapses, the structures that permit neurons to send chemical signals between them.

The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice.

Xu also found that the mice with the same Bdnf mutation grew to be severely obese.

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Gluttony gene that makes you eat more even when you are full identified

London, March 19 (ANI): Scientists have now found answer to why some patients fail to respond to some of the most successful cancer drugs.

Tyrosine kinase inhibitor drugs (TKIs) work effectively in most patients to fight certain blood cell cancers, such as chronic myelogenous leukemia (CML), and non-small-cell lung cancers (NSCLC) with mutations in the EGFR gene.

These precisely targeted drugs shut down molecular pathways that keep these cancers flourishing and include TKIs for treating CML, and the form of NSCLC with EGFR genetic mutations.

Now, a multi-national research team led by scientists at Duke-NUS Graduate Medical School in Singapore, working with the Genome Institute of Singapore (GIS), Singapore General Hospital and the National Cancer Centre Singapore, has discovered that there is a common variation in the BIM gene in people of East Asian descent that contributes to some patients' failure to benefit from these tyrosine kinase inhibitor drugs.

"Because we could determine in cells how the BIM gene variant caused TKI resistance, we were able to devise a strategy to overcome it," said S. Tiong Ong, M.B.B. Ch., senior author of the study and associate professor in the Cancer and Stem Cell Biology Signature Research Programme at Duke-NUS and Division of Medical Oncology, Department of Medicine, at Duke University Medical Center.

"A novel class of drugs called the BH3-mimetics provided the answer," he said.

"When the BH3 drugs were added to the TKI therapy in experiments conducted on cancer cells with the BIM gene variant, we were able to overcome the resistance conferred by the gene. Our next step will be to bring this to clinical trials with patients," Ong added.

Yijun Ruan, Ph.D., a co-senior author of this study and associate director for Genome Technology and Biology at GIS said: "We used a genome-wide sequencing approach to specifically look for structural changes in the DNA of patient samples. This helped in the discovery of the East Asian BIM gene variant. What's more gratifying is that this collaboration validates the use of basic genomic technology to make clinically important discoveries."

If the drug combination does override TKI resistance in people, this will be good news for those with the BIM gene variant, which occurs in about 15 percent of the typical East Asian population. By contrast, no people of European or African ancestry were found to have this gene variant.

"While it's interesting to learn about this ethnic difference for the mutation, the greater significance of the finding is that the same principle may apply for other populations," said Patrick Casey, Ph.D., senior vice dean for research at Duke-NUS and James B. Duke Professor of Pharmacology and Cancer Biology.

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Gene variant in East Asians could explain resistance to cancer drugs

London, March 19 (IANS) Scientists have stumbled on a 'gluttony gene' that converts you into an eating machine even if you are full.

Mice tests have demonstrated that a mutation on a single gene broke down body-brain communication and triggered non-stop eating and rapid weight gain.

But the good news is that the scientists hope identifying the Bdnf gene could help with slimming treatments as obesity is becoming a global epidemic, the journal Nature Medicine reports.

Baoki Xu, who led the study at Georgetown University Medical Centre, US on variations in the Bdnf gene in mice, said: "This discovery may open up novel strategies to help the brain control body weight."

His team found the Bdnf gene has 'short' and 'long' versions which form at an early stage in the womb. Those with the 'long' form sent the chemical signals to say 'I'm full' through a 'superhighway' of neurons in the brain to the hypothalamus, according to the Daily Mail.

In those with the short form, signals reached some brain cells but could not be picked up by the dendrites - the branch-like 'fingers' coming out of the cells which pass messages on to the right place.

Xu said: "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 the appetite is not modified." The mice ate twice as much as those without the mutation.

Humans also have this gene and it has been linked to obesity, but the researchers say it was not clear until now exactly how it worked.

After a meal, the activity of this gene transmits chemical signals down a chain of brain cells until they reach the hypothalamus, which receives the message that you are full and suppresses the appetite.

Scientists will now be looking at whether the faulty transmission line can be modified, to help prevent and treat obesity.

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'Gluttony gene' forces you to gobble non-stop

ScienceDaily (Mar. 18, 2012) Researchers at Georgetown University Medical Center have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain. What results is obesity caused by a voracious appetite.

Their study, published March 18th on Nature Medicine's website, suggests there might be a way to stimulate expression of that gene to treat obesity caused by uncontrolled eating.

The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain. In humans, these hormones, which are released in the body after a person eats, 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," says the study's senior investigator, Baoji Xu, Ph.D., an associate professor of pharmacology and physiology at Georgetown.

"This discovery may open up novel strategies to help the brain control body weight," he says.

Xu has long investigated the Bdnf gene. He has found that the gene produces a growth factor that controls communication between neurons.

For example, he has shown that during development, BDNF is important to the formation and maturation of synapses, the structures that permit neurons to send chemical signals between them. The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice.

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, in fact, linked to obesity.

But, until this study, no one has been able to describe exactly how BDNF controls body weight.

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How a single gene mutation leads to uncontrolled obesity

Editor's Choice Academic Journal Main Category: Obesity / Weight Loss / Fitness Also Included In: Genetics;Neurology / Neuroscience Article Date: 19 Mar 2012 - 11:00 PDT

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The researchers found that the mutation in the Bdnf (brain-derived neurotrophic factor) gene undermines brain neurons' ability to pass insulin and leptin chemical signals through the brain. Their study involved mice.

When a human being has eaten, leptin and insulin are released into the body and literally tell the body to stop consuming food. However, if the signals do not reach parts of the brain they are supposed to - within the hypothalamus - the person will continue feeling hungry, and will carry on eating.

Baoji Xu, Ph.D., said:

Dr. Xu has been carrying out research on the Bdnf gene for years. He explains that this gene produces a growth factor that regulates how neurons communicate with each other.

Xu has demonstrated that during development, BDNF plays a major role in the formation and maturity of synapses. A synapse is the point where two nerve cells connect; a specialized junction at which a neuron (nerve cell) communicates with a target cell - this is done via chemical signals. The Bdnf gene produces one short and one long transcript. When the long-form BdnfN transcript is not there, the growth factor BDNF is only produced in the body of the neuron, but not in its dendrites. This results in the production of too many immature synapses, which undermines learning and memory in mice.

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Gene Mutation Causes Uncontrolled Obesity