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journal of clinical investigation

An international group of scientists have solved the mystery of a genetic flaw which greatly increases the risk of obesity in one in six people.

A version of an obesity gene, called FTO, had been linked to a bigger belly, but the reason why was uncertain.

A study, published in The Journal of Clinical Investigation, showed FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin.

Obesity experts said drugs targeting ghrelin might reduce weight gain.

There is a strong family link with obesity, and a person’s genetic code is thought to play a major role in the risk of them becoming overweight.

People have two copies of the FTO gene – one from each parent – and each copy comes in a high and a low-risk form. Those with two-high risk copies of the FTO gene are thought to be 70% more likely to become obese than those with low-risk genes.

But no-one knew why.

FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin

FTO gene made fatty foods more tempting and altered levels of the hunger hormone, ghrelin

A team, led by researchers at University College London, tested two groups of men. All were a normal weight, but one group had the high-risk FTO genes and the other was low risk.

The first tests looked at levels of the hormone ghrelin either side of a meal in 10 men from each group.

Levels of the hormone, which makes people hungry, did not fall as far in the high-risk patients after the meal. Their ghrelin levels also began to climb more quickly.

In separate tests, a series of brain scans after a meal showed further differences between the two groups. Men with the high-risk genes found pictures of high-fat foods more appealing than the low-risk men.

Dr. Rachel Batterham, the head of the centre for obesity research at University College London, said: “Their brain is set up to be particularly interested in anything to do with high-calorie food.”

She said they were “biologically programmed to eat more”.

Dr. Rachel Batterham said understanding how FTO affected the odds of becoming overweight would help patients.

She said exercise such as cycling was an excellent way to lower ghrelin levels and there was a significant amount of research from pharmaceutical companies working on the hormone.

Dr. Rachel Batterham added: “Also protein meals do lower ghrelin more, so anything that suppresses ghrelin is more likely to be effective in FTO patients.”

The FTO mutations were probably life-saving at one point in human history when piling on the pounds in the summer would help people survive the winter.

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Scientists have discovered a keen sense of taste boosts immunity – a breakthrough that could lead to nasal sprays to ward off illness.

People who find some vegetables, such as sprouts and broccoli, unbearably bitter are better at fighting off bugs due to chemicals in their nose, a study shows.

Experiments found they have more receptors that pick up the flavor of these foods – and also work as an early warning system about bacterial invaders.

They were traditionally thought to be located only on the tongue but are now known to be in the linings of the nasal and sinus cavities as well.

And these receptors are involved in activating the body’s natural defences against common infections.

However, almost a third of the population do not have the specific version of the bitter taste receptor gene called TAS2R38 that activates an immune response.

Dr. Noam Cohen, of the University of Pennsylvania in the United States, said: “If you are a supertaster, it is going to be very rare you are going to get sinusitis.”

But he added this bitter-tasting ability does not protect against all infections.

The findings, published in the Journal of Clinical Investigation, could lead to better treatments for chronic rinosinusitis, a condition of constantly inflamed and swollen sinuses which affects up to one in ten people.

Bitterness is the most sensitive of the tastes, and many find it unpleasant, sharp or disagreeable.

Common bitter foods also include marmalade, olives, citrus peel and wild chicory.

In the study the researchers grew cells in lab dishes, forming structures that resembled the multilayered lining of the nose and sinus, to test out how bitter receptors affect the initial stages of the infection process.

Chemicals produced by common bacteria called Pseudomonas aeruginosa activated the TAS2R38 bitter receptor, and caused the hair-like cilia that line the sinuses to start sweeping away microbial intruders.

The activation also resulted in the release into the sinuses of nitric oxide which kills bacteria.

The researchers looked at just one of 25 bitter receptors and it remains to be seen if the others affect the immune system.

In the past researchers have used phenylthiocarbamide (PTC) to identify people with functional bitter receptors.

Those who can taste the chemical are classified as supertasters,

The researchers said people who would say Brussel sprouts taste bitter are likely to be supertasters, having responsive bitter receptors.

The study also suggests supertasters may have a higher risk of chronic sinusitis, and that non-tasters have more upper respiratory infections.

Upon testing nasal tissue samples from patients who had undergone surgery related to sinus problems, the researchers found none of the eleven supertasters had Pseudomonas bacteria in their tissues, whereas seven out of twenty non-tasters had infections.

Dr. Thomas Finger, an expert in taste and smell at the University of Colorado, reviewed the research and said it could lead to an almost cost free test to distinguish supertasters from the more susceptible non-tasters.

He said certain bitter compounds could also be used to activate the immune system.

For example, a bitter nasal spray could be used to ward off an infection in the early stages.

But such potential therapies are a long way off.

Dr. Noam Cohen said his researchers will next look at whether genetics plays a role in people’s responses to sinusitis treatments.

 

Vitamin B3 could be the new weapon in the fight against resistant bugs such as MRSA, a new research has suggested.

US experts found B3, also known as nicotinamide, boosts the ability of immune cells to kill Staphylococcus bacteria.

B3 increases the numbers and efficacy of neutrophils, white blood cells that can kill and eat harmful bugs.

The study, in the Journal of Clinical Investigation, could lead to a “major change in treatment”.

Vitamin B3 was tested on Staphylococcal infections, such as the potentially fatal MRSA (Methicillin-resistant Staphylococcus aureus).

Vitamin B3 was tested on Staphylococcal infections, such as the potentially fatal MRSA

Vitamin B3 was tested on Staphylococcal infections, such as the potentially fatal MRSA

Such infections are found in hospitals and nursing homes, but are also on the rise in prisons, the military and among athletes.

The scientists used extremely high doses of B3 – far higher than that obtained from dietary sources – in their tests, carried out both on animals and on human blood.

And the researchers say there is as yet no evidence that dietary B3 or supplements could prevent or treat bacterial infections.

The researchers say B3 appears to be able to “turn on” certain antimicrobial genes, boosting the immune cells’ killing power.

Prof. Adrian Gombart, of Oregon State University’s Linus Pauling Institute, who worked on the research, said: “This is potentially very significant, although we still need to do human studies.

“Antibiotics are wonder drugs, but they face increasing problems with resistance by various types of bacteria, especially Staphylococcus aureus.

“This could give us a new way to treat Staph infections that can be deadly, and might be used in combination with current antibiotics.

“It’s a way to tap into the power of the innate immune system and stimulate it to provide a more powerful and natural immune response.”

Prof. Mark Enright, of the University of Bath, said: “Neutrophils are really the front line against infections in the blood and the use of nicotinamide seems safe at this dose to use in patients as it is already licensed for use.

“This could cause a major change in treatment for infections alongside conventional antibiotics to help bolster patients immune system.

“I would like to see in patient clinical trials but cannot see why this couldn’t be used straight away in infected patients.”