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Showing posts with label New England Journal of Medicine. Show all posts
Showing posts with label New England Journal of Medicine. Show all posts

Friday 21 August 2015

Scientists Finally Discover How the Obesity Gene Works



Scientists have finally figured out how the key gene tied to obesity makes people fat, a major discovery that could open the door to an entirely new approach to the problem beyond diet and exercise.

The work solves a big mystery: Since 2007, researchers have known that a gene called FTO was related to obesity, but they didn’t know how, and could not tie it to appetite or other known factors.

Now experiments reveal that a faulty version of the gene causes energy from food to be stored as fat rather than burned. Genetic tinkering in mice and on human cells in the lab suggests this can be reversed, giving hope that a drug or other treatment might be developed to do the same in people.

The work was led by scientists at MIT and Harvard University and published online Wednesday by the New England Journal of Medicine.

The discovery challenges the notion that “when people get obese it was basically their own choice because they choose to eat too much or not exercise,” said study leader Melina Claussnitzer, a genetics specialist at Harvard-affiliated Beth Israel Deaconess Medical Center. “For the first time, genetics has revealed a mechanism in obesity that was not really suspected before” and gives a third explanation or factor that’s involved.

Independent experts praised the discovery.

“It’s a big deal,” said Dr. Clifford Rosen, a scientist at Maine Medical Center Research Institute and an associate editor at the medical journal.

“A lot of people think the obesity epidemic is all about eating too much,” but our fat cells play a role in how food gets used, he said. With this discovery, “you now have a pathway for drugs that can make those fat cells work differently.”

Several obesity drugs are already on the market, but they are generally used for short-term weight loss and are aimed at the brain and appetite; they don’t directly target metabolism.

Researchers can’t guess how long it might take before a drug based on the new findings becomes available. But it’s unlikely it would be a magic pill that would enable people to eat anything they want without packing on the pounds. And targeting this fat pathway could affect other things, so a treatment would need rigorous testing to prove safe and effective.

The gene glitch doesn’t explain all obesity. It was found in 44 percent of Europeans but only 5 percent of blacks, so other genes clearly are at work, and food and exercise still matter.

Having the glitch doesn’t destine you to become obese but may predispose you to it. People with two faulty copies of the gene (one from Mom and one from Dad) weighed an average of 7 pounds more than those without them. But some were obviously a lot heavier than that, and even 7 pounds can be the difference between a healthy and an unhealthy weight, said Manolis Kellis, a professor at MIT.

Related: More U.S. Adults Are Now Obese than Overweight

He and Claussnitzer are seeking a patent related to the work. It was done on people in Europe, Sweden and Norway, and funded by the German Research Center for Environmental Health and others, including the U.S. National Institutes of Health.

Researchers can’t guess how long it might take before a drug based on the new findings becomes available. But it’s unlikely it would be a magic pill that would enable people to eat anything they want without packing on the pounds. And targeting this fat pathway could affect other things, so a treatment would need rigorous testing to prove safe and effective.

The gene glitch doesn’t explain all obesity. It was found in 44 percent of Europeans but only 5 percent of blacks, so other genes clearly are at work, and food and exercise still matter.

Having the glitch doesn’t destine you to become obese but may predispose you to it. People with two faulty copies of the gene (one from Mom and one from Dad) weighed an average of 7 pounds more than those without them. But some were obviously a lot heavier than that, and even 7 pounds can be the difference between a healthy and an unhealthy weight, said Manolis Kellis, a professor at MIT.

Related: ‘Healthy Obesity’ Turns Unhealthy Over Time

He and Claussnitzer are seeking a patent related to the work. It was done on people in Europe, Sweden and Norway, and funded by the German Research Center for Environmental Health and others, including the U.S. National Institutes of Health.

“It’s a potential target” for drug development, said Dr. Sam Klein, an obesity researcher at Washington University in St. Louis. He called the work “an amazing study” and “a scientific tour de force.”

Dr. Rudolph Leibel, an obesity expert at Columbia University in New York, used the same term — “tour de force.” Still, some earlier research suggests the FTO gene may influence other aspects of obesity such as behavior and appetite.

“It’s possible there are several mechanisms being affected,” and that fat-burning is not the whole story, he said.

Read This Next: There Are 6 Types Of Obesity — And Each Should Be Treated Differently

- Associated Press

Thursday 9 February 2012

Memory Strengthened by Stimulating Key Site in Brain

ScienceDaily (Feb. 8, 2012) — Ever gone to the movies and forgotten where you parked the car? New UCLA research may one day help you improve your memory.

UCLA neuroscientists have demonstrated that they can strengthen memory in human patients by stimulating a critical junction in the brain. (Credit: © rolffimages / Fotolia)
UCLA neuroscientists have demonstrated that they can strengthen memory in human patients by stimulating a critical junction in the brain. Published in the Feb. 9 edition of the New England Journal of Medicine, the finding could lead to a new method for boosting memory in patients with early Alzheimer's disease.

The UCLA team focused on a brain site called the entorhinal cortex. Considered the doorway to the hippocampus, which helps form and store memories, the entorhinal cortex plays a crucial role in transforming daily experience into lasting memories.

"The entorhinal cortex is the golden gate to the brain's memory mainframe," explained senior author Dr. Itzhak Fried, professor of neurosurgery at the David Geffen School of Medicine at UCLA. "Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells must send signals through this hub in order to form memories that we can later consciously recall."

Fried and his colleagues followed seven epilepsy patients who already had electrodes implanted in their brains to pinpoint the origin of their seizures. The researchers monitored the electrodes to record neuron activity as memories were being formed.



Using a video game featuring a taxi cab, virtual passengers and a cyber city, the researchers tested whether deep-brain stimulation of the entorhinal cortex or the hippocampus altered recall. Patients played the role of cab drivers who picked up passengers and traveled across town to deliver them to one of six requested shops.

"When we stimulated the nerve fibers in the patients' entorhinal cortex during learning, they later recognized landmarks and navigated the routes more quickly," said Fried. "They even learned to take shortcuts, reflecting improved spatial memory.

"Critically, it was the stimulation at the gateway into the hippocampus - and not the hippocampus itself - that proved effective," he added.

The use of stimulation only during the learning phase suggests that patients need not undergo continuous stimulation to boost their memory, but only when they are trying to learn important information, Fried noted. This may lead the way to neuro-prosthetic devices that can switch on during specific stages of information processing or daily tasks.

Six million Americans and 30 million people worldwide are newly diagnosed with Alzheimer's disease each year. The progressive disorder is the sixth leading cause of death in the United States and the fifth leading cause of death for those aged 65 and older.

"Losing our ability to remember recent events and form new memories is one of the most dreaded afflictions of the human condition," said Fried. "Our preliminary results provide evidence supporting a possible mechanism for enhancing memory, particularly as people age or suffer from early dementia. At the same time, we studied a small sample of patients, so our results should be interpreted with caution."

Future studies will determine whether deep-brain stimulation can enhance other types of recall, such as verbal and autobiographical memories. No adverse effects of the stimulation were reported by the seven patients.

Fried's coauthors included first author Nanthia Suthana, as well as Dr. Zulfi Haneef, Dr. John Stern, Roy Mukamel, Eric Behnke and Barbara Knowlton, all of UCLA. The research was supported by grants from the National Institute of Neurological Disorders and Stroke and the Dana Foundation.


Story Source:
The above story is reprinted from materials provided by University of California, Los Angeles (UCLA), Health Sciences, via Newswise. The original article was written by Elaine Schmidt.
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Journal Reference:
  1. Nanthia Suthana, Zulfi Haneef, John Stern, Roy Mukamel, Eric Behnke, Barbara Knowlton, Itzhak Fried. Memory Enhancement and Deep-Brain Stimulation of the Entorhinal Area. New England Journal of Medicine, 2012; 366 (6): 502 DOI: 10.1056/NEJMoa1107212
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