This research by IIT Mandi has shown that excessive sugar intake leads to a fatty liver. This should offer incentive to the public to reduce sugar intake to stop NAFLD in its early stages
A team of researchers from IIT Mandi has established the underlying bio-chemical relationship between the consumption of excessive sugar and the development of ‘fatty liver,’ medically known as Non-Alcoholic Fatty Liver Disease (NAFLD), a statement from the institute informed.
The research comes at a time when the Government of India has included NAFLD in the National Programme for Prevention and Control of Cancer, Diabetes, Cardiovascular Diseases and Stroke (NPCDCS).
Explaining his research, Dr Prosenjit Mondal, Associate Professor – School of Basic Sciences, IIT Mandi, said, “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 the fatty liver through De Novo Lipogenesis (DNL).”
India is the first country in the world to identify the need for action on NAFLD and with good reason. The prevalence of NAFLD in India is in about nine per cent to 32 per cent of the population, with the state of Kerala alone having a prevalence of 49 per cent and a staggering 60 per cent prevalence among obese school-going children.
One of the causes for 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 in a process called hepatic DNL, which leads to fat accumulation in the liver.
Through a complementary experimental approach involving mice models, the IIT Mandi team has shown the hitherto unknown link between the carbohydrate-induced activation of a protein complex called NF-κB and increased DNL.
“Our data indicates that the sugar-mediated shuttling of hepatic NF-κB p65 reduces the levels of another protein, sorcin, which, in turn, activates liver DNL through a cascading bio-chemical pathway,” explained the lead scientist.
The unravelling of the molecular link between sugar and fat accumulation in the liver is key to developing therapeutics for the disease. The team has shown that drugs that can inhibit NF-κB can prevent sugar-induced hepatic fat accumulation. They have also shown that the knockdown of sorcin reduces the lipid-lowering ability of the NF-κB inhibitor.
The IIT Mandi team’s finding that NF-κB plays a key role in lipid accumulation in the liver opens up a new avenue of therapeutics for NAFLD. NF-κB also plays a role in other diseases that involve inflammation, such as cancer, Alzheimer’s disease, atherosclerosis, IBS, stroke, muscle wasting and infections, and scientists around the world are developing therapeutics that can block NF-κB. The research shows that NAFLD can now be added to the repertoire of diseases that can be treated with drugs that block NF-κB.
From the preventive angle, the research has conclusively shown that excessive sugar intake leads to a fatty liver. This should offer incentive to the public to reduce sugar intake to stop NAFLD in its early stages.
The results of the team’s work have been published in the Journal of Biological Chemistry. The research paper has been co-authored by Dr Mondal, along with his research scholars Vineeth Daniel, Surbhi Dogra, Priya Rawat, Abhinav Choubey from IIT Mandi, in collaboration with Dr Mohan Kamthan and Aiysha Siddiq Khan from Jamia Hamdard Institute, New Delhi and Sangam Rajak from Sanjay Gandhi Post Graduate Institute of Medical Sciences (SGPGI), Lucknow.
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