Pages

Do YOU have the 'fat gene'? 90% of obese people could have mutation that means they're programmed to eat more and move less.

Friday, November 22, 2013

ADS
Scientists believe as many as nine in 10 obese people are fat because of their genes
Scientists believe as many as nine in 10 obese people are fat because of their genes
Spending hours in the gym to stay slim may be all for nothing if you have the wrong genes, a new study suggests.
Scientists believe as many as nine in 10 obese people are fat because of their genes.
They say the ‘fat gene’ is so powerful that when it mutates it makes mice twice as fat, and diabetic.
By looking at just one family, scientists were able to pinpoint the defective gene – known as CEP19 - that caused them to be obese.
The team from the Icahn School of Medicine in the U.S. found that ‘switching off’ the gene in mice caused them to become morbidly obese by making them want to eat more and burn off fewer calories.
They believe the gene plays a vital role in determining appetite and energy levels.
This means that when it is functioning normally it helps people stay lean.
However, when it mutates, it can cause energy levels to plummet and appetite to increase, resulting in obesity.
Geneticist Dr John Martignetti said: ‘Starting with the gene discovery in a single family with morbid obesity, these studies led to the identification of a gene that seems to be fundamental to regulating nutritional status.
‘This gene is shown to be present not only in humans and mice, but also in the simplest known single-cell animal.
‘Nature considers this gene so important that it has preserved its structure for more than 700 million years.’
The researchers believe therapies to revive the gene in people at risk of obesity could help treat or avert obesity and Type 2 diabetes.
Dr Martignetti and Dr Adel Shalata, of the Ziv Medical Centre, in Israel, found the gene mutation in an obese Israeli family suffering from ‘autosomal-recessive’ morbid obesity and tested the gene's role in mice.
The scientists analysed DNA from blood samples taken from 13 obese and 31 non-obese members of the family living in the same village in northern Israel.
The researchers say the 'fat gene' is so powerful that when it mutates it makes mice twice as fat, and diabetic
The researchers say the 'fat gene' is so powerful that when it mutates it makes mice twice as fat, and diabetic
Affected individuals had an average body mass index (BMI) of 48.7, a figure far above the obesity threshold of 30 that put them into the ‘morbidly obese’ category. The BMI range of obese family members varied from 36.7 to 61.
The analysis revealed a mutation in a gene which can lead to diseases affecting the kidney, liver, pancreas and bones, as well as obesity.
When scientists deleted a version of the CEP19 gene in laboratory mice, the animals became obese and diabetic, and developed increased appetites. Their energy expenditure decreased, and their ability to break down fat was impaired.
The gene plays a vital role in determining appetite and energy levels meaning when it is functioning normally it helps people stay lean. When it mutates it can cause energy levels to plummet and appetite to increase, resulting in obesity
The gene plays a vital role in determining appetite and energy levels meaning when it is functioning normally it helps people stay lean. When it mutates it can cause energy levels to plummet and appetite to increase
Dr Martignetti said: ‘The mouse models we have generated, which can be more than twice as heavy as other mice and are insulin resistant, represent important research tools for basic biology and clinical testing.’
Gene therapy could hold the answer to fighting the obesity epidemic, they claim.
Dr Martignetti added: ‘Obesity is a global epidemic, affecting almost all areas of human health, from heart disease to cancer, and impacting upon most of the major causes of preventable death.
‘Moreover, obesity rates are rising dramatically worldwide. If we are going to combat this disease, we need to understand its medical basis.’
ADS

No comments:

Post a Comment

 

Most Reading

Archives