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abbages 'cut lung cancer risks'

cabbage

The researchers looked at how much cabbage people ate

Eating vegetables from the cabbage family can reduce the risk of lung cancer

for people with a certain genetic make-up, scientists say.

 

Such cruciferous vegetables had already been linked to reduced rates of lung

cancer, but it had not been clear why.

 

The study found eating the vegetables at least once a week cut cancer risk

for people with inactive versions of two genes, carried by 70% of people.

 

The Lancet study was by International Agency for Cancer Research scientists.

 

http://news.bbc.co.uk/1/hi/health/4382142.stm

 

 

Way to beat dieters' hunger pangs

Image of a man eating

Drug manufacturers are looking at ways to suppress appetite

Scientists believe they are closer to understanding how to control appetite.

 

Two studies in Science magazine look at brain cells, and their signals, that

appear to drive weight loss and suppress hunger.

 

Killing off particular neurons or boosting a protein that keeps neurons

alive makes mice lose weight by eating less.

 

The US teams from Boston and Seattle say the similar appetite pathways are

present in humans.

 

Appetite control

 

Scientists have already been trying to develop weight-loss drugs that act on

these brain pathways.

 

The first study in Science looked at a compound called ciliary neurotrophic

factor (CNTF). This protein has been shown to cause weight loss in both

humans and mice.

 

It is thought to work by blocking the hunger signals that stimulate

appetite, but its exact action is not clear.

 

 

These papers suggest that switching NPY neurones off could cure obesity

Experts from Imperial College London

 

Dr Maia Kokoeva and colleagues at Harvard Medical School looked what

happened when they gave CNTF to mice.

 

CNTF prompted the growth of new neurons in an area of the brain called the

hypothalamus, which plays a crucial role in controlling appetite and energy

balance.

 

They believe that CNTF has a dual action. During treatment it activates a

pathway in the hypothalamus that makes the brain more responsive to the

hormone leptin, which is made by fat cells and tells the body how well fed

it is.

 

By triggering the growth of more leptin-responsive neurons, it also makes

the body more sensitive to leptin even after the treatment is stopped, they

told Science.

 

No hunger

 

The second study, by a team at the University of Washington, looked at the

neurons involved in appetite - POMC and NPY/AgRP.

 

POMC neurons are know to send signals to the brain to reduce appetite and

mice with defects in these neurons eat excessively and become obese.

 

In comparison, when the researchers eliminated NPY/AgRP neurons in adult

mice the animals began to eat less and less, suggesting these neurons act in

opposition to POMC.

 

However, when they killed off the NPY/AgRP neurons in baby mice these

animals continued to eat normally and maintained a normal body weight.

 

The findings suggest that if NPY/AgRP neurons are eliminated before they

become fully functional, then animals somehow compensate.

 

Lead researcher Dr Richard Palmiter said: "Everybody in the field believes

that NPY/AgRP neurons and POMC neurons are undoubtedly doing the same in

humans as they do in rodents. So I would predict that if you could do the

experiment in humans, the results would be the same."

 

He believes that mutations in human genes that affect the survival of these

neurons or their ability to respond to hormonal signals could explain why

some people are naturally very thin and others are overweight.

 

Dr Gavin Bewick, Dr James Gardiner and Professor Steven Bloom at Imperial

College London, UK, have been looking at NYP/AgRP and were the first to

demonstrate that loss of these neurons leads to reduced appetite and weight.

 

They said: "We are at last beginning to understand how the brain works.

Together these papers suggest that switching NPY neurones off could cure

obesity."

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