City scientists uncover liver protein managing fat storage
Kolkata: In a paper published in the international journal Nature Communications, a team of scientists from the Saha Institute of Nuclear Physics, Kolkata, that operates under the department of atomic energy, discovered a tiny protein inside liver cells called TCF19 that acts like a traffic controller for fat. The scientists found that when the human liver is flooded with harmful fat, the kind that can damage cells, TCF19 steps in and converts it into a safer, more stable form of fat called triglycerides, which can be stored without causing harm. It buys the liver time and slows the progression to severe disease.
In the past five years, a team of four researchers from the institute’s Biophysical Science Division, headed by Professor Chandrima Das, worked to “uncover a hidden molecular mechanism that plays a dual role, both protecting the liver and contributing to the onset of the disease.” Their research turned the spotlight on how the liver adapts to stress induced by modern lifestyles, especially high-fat diets and sedentary behaviour.
“Our work centres on non-alcoholic fatty liver disease (NAFLD), a condition that has emerged as a major public health concern. Affecting one in three adults, this disease is closely associated with obesity, type 2 diabetes and cardiovascular disorders and often remains undetected until it advances to severe liver damage,” said Das.
The research fellows of the institute, who worked under Das, are Atanu Mondal, Sandhik Nandi and Vipin Singh. “The focal point of this research is that the TCF19 protein acts as a gatekeeper to regulate fatty liver to fibrosis transition, a condition when liver becomes stiff, and this raises the chance of liver failure or liver cancer. Our study began with an organoid model and then we experimented on 40-60 animals and conducted clinical tests on 70 people with the help of doctors. The animal experiments were conducted using the facility of IISER Pune,” Das told TOI.
According to Mondal, a senior research fellow at the institute, the finding reveals how the body’s defence system can slow down the progression of the disease. “We found that when the liver is exposed to toxic lipid stress, it helps convert harmful lipid species into triglycerides, a relatively safer storage form. This adaptive mechanism protects the liver and delays progression to more severe stages of disease like fibrosis. The same protective response also promotes the accumulation of fat within the liver, thereby indicating the early phases of NAFLD,” said Mondal.
According to Das, the study suggests that a more effective strategy may lie in fine-tuning how lipids are processed and balanced within liver cells. “By shifting the focus from simple fat reduction to metabolic regulation, the research opens new avenues for targeted and nuanced interventions. As NAFLD continues to rise sharply among urban population due to lifestyle changes, this work attempts to provide critical insights on liver diseases,” she said.
“Our work centres on non-alcoholic fatty liver disease (NAFLD), a condition that has emerged as a major public health concern. Affecting one in three adults, this disease is closely associated with obesity, type 2 diabetes and cardiovascular disorders and often remains undetected until it advances to severe liver damage,” said Das.
The research fellows of the institute, who worked under Das, are Atanu Mondal, Sandhik Nandi and Vipin Singh. “The focal point of this research is that the TCF19 protein acts as a gatekeeper to regulate fatty liver to fibrosis transition, a condition when liver becomes stiff, and this raises the chance of liver failure or liver cancer. Our study began with an organoid model and then we experimented on 40-60 animals and conducted clinical tests on 70 people with the help of doctors. The animal experiments were conducted using the facility of IISER Pune,” Das told TOI.
According to Mondal, a senior research fellow at the institute, the finding reveals how the body’s defence system can slow down the progression of the disease. “We found that when the liver is exposed to toxic lipid stress, it helps convert harmful lipid species into triglycerides, a relatively safer storage form. This adaptive mechanism protects the liver and delays progression to more severe stages of disease like fibrosis. The same protective response also promotes the accumulation of fat within the liver, thereby indicating the early phases of NAFLD,” said Mondal.
According to Das, the study suggests that a more effective strategy may lie in fine-tuning how lipids are processed and balanced within liver cells. “By shifting the focus from simple fat reduction to metabolic regulation, the research opens new avenues for targeted and nuanced interventions. As NAFLD continues to rise sharply among urban population due to lifestyle changes, this work attempts to provide critical insights on liver diseases,” she said.
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