Non-alcoholic fatty liver disease affects more than 30 per cent adult Indians.
Kolkata:
Advancing the hunt for elusive therapeutics against non-alcoholic fatty liver disease (NAFLD), the most common liver affliction across the globe, the Indian researchers have discovered a new mechanism through which the liver hoards up extra fat from sources other than alcohol.
They have also identified a brand new drug target for potential therapy for the disease, that tends to develop in people who are overweight or obese or have type-2 diabetes.
NAFLD affects more than 30 per cent adult Indians and occurs when more than 5 to 10 per cent of the liver's weight is fat.
There is no definite therapy for the disease.
Moreover, a significant number of NAFLD patients progress to the most extreme form of the disease called non-alcoholic steatohepatitis (NASH), an irreversible clinical condition that causes the liver to swell and become damaged and trigger cirrhosis in adults.
The senior researcher Partha Chakrabarti's research group along with Saikat Chakrabarti's laboratory at Indian Institute of Chemical Biology, a unit of CSIR, decided to take a shot at the silent, crippling disease that evolves over decades, its prevalence advantaged with low public awareness.
They literally copped their eyes on to the cell's protein degradation machinery to zero-in on the target protein COP1.
"Multiple molecular mechanisms believed to cause NAFLD have been put forward over the years. However, we identified a hitherto unknown mechanism for the control of liver fat," Chakrabarti, Cell Biology & Physiology Division at the institute told IANS.
"We find that inhibition of COP1 can significantly reduce liver fat in NAFLD. However, it is still not clear whether COP1 can halt disease progression or can prevent NASH. We are currently working in this direction," Chakrabarti added.
The study has been published in September in the journal Diabetes, from American Diabetes Association (ADA).
According to CSIR-IICB Director Samit Chattopadhyay, the development will motivate the scientific community to come up with new solutions to this global problem and is "geared towards India's goal of delivering translational research outputs to the nation."
They have also identified a brand new drug target for potential therapy for the disease, that tends to develop in people who are overweight or obese or have type-2 diabetes.
NAFLD affects more than 30 per cent adult Indians and occurs when more than 5 to 10 per cent of the liver's weight is fat.
There is no definite therapy for the disease.
Moreover, a significant number of NAFLD patients progress to the most extreme form of the disease called non-alcoholic steatohepatitis (NASH), an irreversible clinical condition that causes the liver to swell and become damaged and trigger cirrhosis in adults.
The senior researcher Partha Chakrabarti's research group along with Saikat Chakrabarti's laboratory at Indian Institute of Chemical Biology, a unit of CSIR, decided to take a shot at the silent, crippling disease that evolves over decades, its prevalence advantaged with low public awareness.
They literally copped their eyes on to the cell's protein degradation machinery to zero-in on the target protein COP1.
"Multiple molecular mechanisms believed to cause NAFLD have been put forward over the years. However, we identified a hitherto unknown mechanism for the control of liver fat," Chakrabarti, Cell Biology & Physiology Division at the institute told IANS.
"We find that inhibition of COP1 can significantly reduce liver fat in NAFLD. However, it is still not clear whether COP1 can halt disease progression or can prevent NASH. We are currently working in this direction," Chakrabarti added.
The study has been published in September in the journal Diabetes, from American Diabetes Association (ADA).
According to CSIR-IICB Director Samit Chattopadhyay, the development will motivate the scientific community to come up with new solutions to this global problem and is "geared towards India's goal of delivering translational research outputs to the nation."
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