A slimming pill to combat obesity is one step closer after scientists discovered two genes that make people fat. The so-called ‘fat genes’ affect the production of another gene, which plays a role in whether fat is stored in the body or burnt off as heat. Mice genetically engineered to lack the Cnot7 and Tob genes remained lean even after gorging themselves, researchers found. It is now hoped the findings will one day be used to aid the development of anti-obesity drugs or ‘slimming pills’. Such a drug would also reduce the risk of a host of other killer illnesses, including heart disease, cancer and type 2 diabetes. Lead researcher Dr Takahashi Akinori, of the Okinawa Institute of Science and Technology Graduate University, said the key was establishing how to encourage the body to burn fat as heat. ‘We wish to inhibit the pathway that suppresses the conversion of fat into heat,’ he said. ‘Being able to enhance fat burning could have clinical applications, such as the production of anti-obesity drugs.’
The growing number of people who are overweight or obese is among the world’s major health concerns. The World Health Organisation warns worldwide obesity has more than doubled since 1980. In 2014, more than 1.9 billion adults, 18 years and older, were overweight. Of these over 600 million were obese, it said. Although there is an urgent need for a cure obesity, there is no safe and effective medical treatment available, and measures are limited to individual efforts, such as sticking to a healthy lifestyle and dietary restrictions, Dr Akinori said.
His research analyses the causes of obesity at a genetic level and looks at one of the molecular mechanisms involved in storing and burning fat. He found the ‘fat genes’ – known as Cnot7 and Tob – affected the activity of another gene, called Ucp1. The Ucp1 gene controls the production of a protein by the same name that is sent into fat cells. In humans, this helps burn off the pounds by converting fat into heat. It is well known obese people and mice have low concentrations of Ucp1 in fat, which makes them prone to storing it instead.
Slimming pills to prevent obesity would also reduce the risk of a host of other killer illnesses, including heart disease, cancer and type 2 diabetes+2. Slimming pills to prevent obesity would also reduce the risk of a host of other killer illnesses, including heart disease, cancer and type 2 diabetes. The study found that mice without the ‘fat genes’ stayed slim even after eating a high fat diet because they are related to the way Ucp1 works. In order to supply fat cells with Ucp1 protein, the Ucp1 gene has to be transcribed into another molecule called messenger RNA, or mRNA. Ucp1 mRNA controls the total amount of Ucp1 protein available in cells, and ultimately, whether more fat is stored in the body or not. Low levels of Ucp1 protein makes cells prone to storing fat, whereas high levels encourages them to burn it as energy instead.
In obese mice, the ‘fat genes’ Cnot7 and Tob degrade Ucp1 mRNA, so that it can no longer be used to make Ucp1 protein, so less is sent into cells to be used by the body, causing more fat to be stored. Conversely, mice bred to lack Cnot7 and Tob produce Ucp1 mRNA in stable amounts, and more Ucp1 protein is sent into cells. As a result, their fat is burned off and they do not become obese, even on a high-fat diet. The researchers are now planning to take the study to another level, with the ultimate aim of developing drugs that act on Cno7 and Tob to prevent obesity. The findings were published in the journal Cell Reports. ( By Madlen Davies from Dailymail.co.uk )