Cellular pathway linked to obesity-related disorders `found`

Washington: Scientists, led by an Indian- origin researcher, claim to have found a certain cellular pathway which is linked to obesity-related disorders like diabetes, heart disease and fatty liver disease.

Tapan Chatterjee and colleagues at the University of Cincinnati says its findings could lead to a potential molecular target for metabolic diseases in humans.

They found that genetically "deleting" the enzyme histone deacetylase 9 (HDAC9) completely protected mice against the health consequences of high-fat feeding, like elevated blood sugar, cholesterol levels and fatty liver disease.

Chatterjee says HDAC9 has been found to lead to obesity- induced body fat dysfunction.
"Failure of fat cells to differentiate and properly store excess calories in obesity is associated with adipose tissue (fat) inflammation, fatty liver disease, insulin resistance, diabetes and increased cardiovascular diseases," he said.

"We know that dysfunctional fat tissue is the underlying culprit in obesity-related diseases. Caloric intake promotes HDAC9 down-regulation to allow the conversion of precursor fat cells to functional fat cells, capable of efficiently storing excess calories for future use and also maintaining whole-body lipid and glucose stability.

"Unfortunately, during chronic over-feeding, the HDAC9 level is up-regulated in fat tissue, thereby blocking the conversion which leads to adipose tissue dysfunction and the onset of diseases such as diabetes, liver disease, high blood pressure and heart disease," Chatterjee added.

The researchers said that in previous studies, elevated HDAC9 expression in fat cells was found to be the underlying molecular culprit for dysfunctional fat tissue during obesity.

"In this study, deleting the HDAC9 gene completely prevented mice from developing obesity-related diseases during chronic high-fat feeding. These results mean the discovery of a potential molecular culprit in obesity-related disease development," Chatterjee said.


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