Ucp 1 identified as major Fat burning gene at molecular level. The retarded function of the Ucp 1 leads to excessive fat storage in fat cells resulting in obesity.
Obesity is becoming a major health concern for many people throughout the world. Obesity is putting individuals at risk for high blood pressure, heart disease and cancer.
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There are no safe and effective medical treatments for Obesity. Even countermeasures are limited to individual efforts. Researchers at Okinawa Institute of Science and Technology Graduate University (OIST) have a breakthrough.
The researchers have found the causes of obesity at the genetic level. They claim to have discovered one of the molecular mechanisms involved in storing and burning fat.
The research was led by Dr Takahashi Akinori and his colleagues of the OIST Cell Signaling Unit. The results of the research will be published in the December 29th, 2015 issue of the journal: Cell Reports.
According to the OIST team they have discovered that mice lacking 2 genes remain lean even after eating a high-fat diet. The mice lacking genes are known as Cnot7 and Tob.
Researchers found over expression of another gene called Ucp1 keeps them lean. Ucp1 was found to aid in the reduction fat deposits. Ucp 1 works by converting fat stored in fat cells into heat.
Obese people and mice have low concentrations of Ucp1 in their fat cells. Low levels of Ucp 1 leads to increased fat storage rather than burn it off.
Ucp 1, Cnot7 and Tob were found to be functionally related. Ucp 1 is transcribed into an mRNA to supply the fat cells with functional Ucp1 protein.
Stable Ucp1 mRNA and Ucp1 protein occur due to lack of Cnot7 and Tob. People with unstable Ucp1 mRNA are prone to become fat. The instability compromises the fat-burning function of Ucp1.
"We wish to inhibit the pathway that suppresses the conversion of fat into heat. Being able to enhance fat burning could have clinical applications, such as the production of anti-obesity drugs," explains Dr Takahashi.
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These findings by Dr Takahashi Akinori and his colleagues of the OIST Cell Signaling Unit are goign to publish in the December 29, 2015 issue of the journal, Cell Reports.