A team of Indian Institute of Technology-Mandi researchers has unfolded the molecular mechanism by which excess sugar consumption causes fatty liver disease.
The team has used a complementary experimental approach together with mice models, for establishing the biochemical relationship between consuming excessive sugar and forming of fatty liver, clinically known as Non-Alcoholic Fatty Liver Disease (NAFLD).
Prosenjit Mondal, Associate professor for School of Basic Sciences at IIT Mandi explains in a Press Release, that one of the major causes of NAFLD is the excess of sugar both table sugar (sucrose) and other forms of carbohydrates (starches, Fiber). This excess of sugar intake causes the liver to convert it into fat through the process hepatic De Novo Lipogenesis or DNL, leading to fat accumulation in the liver.
Mondal said, "Our data indicate 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 biochemical pathway."
What is NAFLD?
NAFLD is a medical condition where excess fat is deposited in the liver. The disease develops slowly, with no clear symptoms for close to two decades. If not treated early the excess fat can irritate the liver cells, resulting in scarring of the liver (cirrhosis). In advanced cases when treatment becomes difficult, it can lead to liver cancer.
As the team suggests in the Press release, the research might urge the public to reduce sugar intake in daily living to prevent NAFLD in its outset. Mondal mentions that in India is found in about 9 per cent to 32 per cent of the population has NAFLD. Kerala alone has a prevalence rate of 49 per cent and is common among obese school-going children(60 per cent)
Treatment of NAFLD
The team includes experienced scholars Vneeth Daniel, Surbhi Dogra, Priya Rawat, Abhinav Choubey from IIT Mandi, Mohan Kamthan, and Aiysha Siddiq Khan and Sangam Rajak from Jamia Hamdard Institute and SGPGI, Lucknow respectively. They claim that this research can prove effective for developing therapeutics for the disease. The team suggests that drugs that have the capacity to inhibit NF-κB can prevent sugar-induced hepatic fat accumulation. But they add that the knockdown of sorcin will reduce the lipid-lowering ability of the NF-κB inhibitor.
The research results are revealed 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) This evolutionary study has been published in the Journal of Biological Chemist.
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