A group of researchers from the Indian Institute of Technology (IIT), Mandi has unravelled the molecular mechanism by which extra sugar consumption causes fatty liver illness.

According to the group, the analysis will immediate the general public to scale back sugar consumption to cease Non-Alcoholic Fatty Liver Disease (NAFLD) in its early phases.

The analysis, which comes at a time when the federal government has included NAFLD within the National Programme for Prevention and Control of Cancer, Diabetes, Cardiovascular Diseases and Stroke (NPCDCS), has been printed within the Journal of Biological Chemistry.

NAFLD is a medical situation through which extra fats deposits within the liver. The illness begins silently, with no overt signs for so long as 20 years. If left untreated, the surplus fats can irritate the liver cells, leading to scarring of the liver (cirrhosis). In superior instances, it could actually additionally result in liver most cancers.

“One of the causes of NAFLD is the overconsumption of sugar — both table sugar (sucrose) and other forms of carbohydrates. The consumption of excess sugar and carbohydrates causes the liver to convert them into fat through a process called hepatic De Novo Lipogenesis or DNL, which leads to fat accumulation in the liver,” stated Prosenjit Mondal, affiliate professor, School of Basic Sciences, IIT Mandi.

“The molecular mechanisms that increase hepatic DNL due to overconsumption of sugar have not been clear. Our goal was to unravel this mechanistic pathway between excessive sugar consumption and onset and development of fatty liver through DNL,” he stated.

Mondal stated the prevalence of NAFLD in India is present in about 9 per cent to 32 per cent of the inhabitants. Kerala alone has a prevalence fee of 49 per cent. There is a staggering 60 per cent prevalence fee amongst overweight school-going kids.

“Through a complementary experimental approach involving mice models, the team has shown the hitherto unknown link between the carbohydrate-induced activation of a protein complex called NF-κB and increased DNL.

“Our knowledge signifies that the sugar-mediated shuttling of hepatic NF-κB p65 reduces the degrees of one other protein, sorcin, which in flip prompts liver DNL by way of a cascading biochemical pathway,” he said.

The research team claimed that unravelling the molecular link between sugar and fat accumulation in the liver is key to developing therapeutics for the disease.

“The group has proven that medicine that may inhibit NF-κB can forestall sugar-induced hepatic fats accumulation. They have additionally proven that the knockdown of sorcin reduces the lipid-lowering means of the NF-κB inhibitor,” Mondal said.

“From the preventive angle, the IIT Mandi group’s analysis has conclusively proven that extreme sugar consumption results in a fatty liver. This ought to supply an incentive to the general public to scale back sugar consumption to cease NAFLD in its early phases,” he stated.

The different members of the analysis group embrace analysis students Vineeth Daniel, Surbhi Dogra, Priya Rawat, Abhinav Choubey from IIT Mandi, Mohan Kamthan and Aiysha Siddiq Khan from Jamia Hamdard Institute and Sangam Rajak from SGPGI, Lucknow.

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