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Study reveals that excess sugar intake causes fatty liver

Recently, a team of researchers from the Indian Institute of Technology (IIT), Mandi have unravelled the molecular mechanism by which excess sugar consumption causes fatty liver disease.

According to the team, the research will prompt the public to reduce sugar intake to stop Non-Alcoholic Fatty Liver Disease (NAFLD) in its initial stages.

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

NAFLD is a medical condition in which excess fat deposits in the liver. The disease starts silently, with no overt symptoms for as long as two decades. If left untreated, the excess fat can irritate the liver cells, resulting in scarring of the liver (cirrhosis). In advanced cases, it can also pave way to liver cancer.

‘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,’ said Prosenjit Mondal, Associate Professor, School of Basic Sciences, IIT Mandi.

‘The molecular mechanisms that increase hepatic DNL due to overconsumption of sugar has 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 said.

Mondal further said that the prevalence of NAFLD in India is found in about 9 per cent to 32 per cent of the population. Kerala alone has a prevalence rate of 49 per cent. There is a staggering 60 per cent prevalence rate among obese school-going children.

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-kB and increased DNL.

‘Our data indicates that the sugar-mediated shuttling of hepatic NF-kB p65 reduces the levels of another protein, sorcin, which in turn activates liver DNL through a cascading biochemical pathway,’ he said.

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

‘The team has shown that drugs that can inhibit NF-kB can prevent sugar-induced hepatic fat accumulation. They have also shown that the knockdown of sorcin reduces the lipid-lowering ability of the NF-kB inhibitor,’ he added.

‘From the preventive angle, the IIT Mandi team’s research has shown that excessive sugar intake leads to a fatty liver. This should offer an incentive to the public to reduce sugar intake to stop NAFLD in its initial stages,’ he further added.

The other members of the research team include research scholars 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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