The
scientists, led by a researcher of Indian origin say they have found a
safe route to the cell diseases such as obesity, diabetes, heart
disease and fatty liver is associated.
Tapan Chatterjee and his colleagues at the University of Cincinnati say that their findings could be a potential target for molecular metabolic disease in humans.
We found that the "Delete" genetically the enzyme histone deacetylase 9 (HDAC9) completely protected mice against the health effects of diets high in fat, such as hyperglycemia, liver disease, high cholesterol and fatty acid.
Chatterjee said HDAC9 was found to lead to obesity-induced dysfunction of body fat. "Failure to differentiate from fat cells and store them properly in obesity is excess calories to fatty tissue (fat), inflammation, fatty liver, insulin resistance, diabetes and the associated increased cardiovascular disease," he said.
"We know that dysfunctional fat tissue is the culprit induced behind the obesity disease. Caloric intake promotes HDAC9 down-regulation, the conversion of fat precursor cells allowing fat cells functional, able to efficiently store the excess calories for future use and maintenance of the whole body lipid and the stability of the glucose.
"Unfortunately, in the history of the food HDAC9 at the level in adipose tissue, the transformation that leads to dysfunction of adipose tissue and regulated by the outbreak of diseases such as diabetes, diseases of the liver is blocked, high blood pressure and heart disease," said Chatterjee.
The researchers said previous studies, high HDAC9 expression was found in the fat cells to be guilty of the underlying molecular dysfunctional adipose tissue in obesity for.
"In this study, deletion of the gene HDAC9 completely prevented mice from developing obesity-related chronic diseases of high fat foods mean. These results, the discovery of a molecular potential culprit in the development of obesity-related diseases," said Chatterjee.
Tapan Chatterjee and his colleagues at the University of Cincinnati say that their findings could be a potential target for molecular metabolic disease in humans.
We found that the "Delete" genetically the enzyme histone deacetylase 9 (HDAC9) completely protected mice against the health effects of diets high in fat, such as hyperglycemia, liver disease, high cholesterol and fatty acid.
Chatterjee said HDAC9 was found to lead to obesity-induced dysfunction of body fat. "Failure to differentiate from fat cells and store them properly in obesity is excess calories to fatty tissue (fat), inflammation, fatty liver, insulin resistance, diabetes and the associated increased cardiovascular disease," he said.
"We know that dysfunctional fat tissue is the culprit induced behind the obesity disease. Caloric intake promotes HDAC9 down-regulation, the conversion of fat precursor cells allowing fat cells functional, able to efficiently store the excess calories for future use and maintenance of the whole body lipid and the stability of the glucose.
"Unfortunately, in the history of the food HDAC9 at the level in adipose tissue, the transformation that leads to dysfunction of adipose tissue and regulated by the outbreak of diseases such as diabetes, diseases of the liver is blocked, high blood pressure and heart disease," said Chatterjee.
The researchers said previous studies, high HDAC9 expression was found in the fat cells to be guilty of the underlying molecular dysfunctional adipose tissue in obesity for.
"In this study, deletion of the gene HDAC9 completely prevented mice from developing obesity-related chronic diseases of high fat foods mean. These results, the discovery of a molecular potential culprit in the development of obesity-related diseases," said Chatterjee.
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