(The Gist of Science Reporter) IIT Mandi Researchers Discover the Molecular Mechanism by which Excess Sugar Consumption Causes Fatty Liver Disease
(GIST OF SCIENCE REPORTER) IIT Mandi Researchers Discover the Molecular Mechanism by which Excess Sugar Consumption Causes Fatty Liver Disease
IIT Mandi Researchers Discover the Molecular Mechanism by which Excess Sugar Consumption Causes Fatty Liver Disease
A team of researchers from IIT Mandi, has used complementary experimental approaches, to establish the underlying biochemical relationship between the consumption of excessive sugar and the development of ‘fatty liver’, medically known as Non-Alcoholic Fatty Liver Disease (NAFLD).
About the disease:
NAFLD is a medical condition in which excess fat deposits in the liver.
The disease starts silently, with no overt symptoms for as much as two decades. If left untreated, the excess fat can irritate the liver cells, resulting in scarring of the liver (cirrhosis), and in advanced cases, can even lead to liver cancer.
The treatment of advanced stages of NAFLD is difficult.
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 about 9% to 32% of the population, with the state of Kerala alone having a prevalence of 49% and a staggering 60% 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 De Novo Lipogenesis or DNL, which leads to fat accumulation in the liver.
The research team has shown the hitherto unknown link between the carbohydrate-induced activation of a protein complex called NF-κB and increased DNL.
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 research team 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 team shows that NAFLD can now be added to the repertoire of diseases that can be treated with drugs that block NF-κB.