IIT Mandi identifies link between fatty liver and type 2 diabetes

Researchers team at IIT Mandi found a relation between fatty liver disease and type 2 diabetes mellitus (T2DM).

Indian Institute of Technology Mandi's researchers have identified a link between fatty liver disease and type 2 diabetes mellitus (T2DM). This understanding enables newer techniques to diagnose the risk of diabetes among people with non-alcoholic fatty liver disease (NAFLD) and the findings of this research also offer new therapeutic pathways to control or even reverse fatty liver-induced diabetes.

This research is important for India because the prevalence of NAFLD is rapidly increasing in the country and recent surveys show that 40% of Indian adults suffer from it. NAFLD is often associated with Type 2 Diabetes, with nearly 50 million Indian adults having both diseases.

The findings of the research have been published in the Journal Diabetes. The paper has been authored by Dr. Prosenjit Mondal, Associate Professor, School of Biosciences and Bioengineeringalong with his scholars Ms. Surbhi Dogra, Ms. Priya Rawat, Dr. P Vineeth Daniel and In collaboration with Dr. Partha Chakrabarti from CSIR-Indian Institute of Chemical Biology, Kolkata, Dr. Debajyoti Das, Mr Sujay K. Maity, Mr Avishek Paul along with Dr. Dr. Kausik Das,and Dr. Souveek Mitra from IPGMER and SSKM Hospital, Kolkata, said IIT Mandi's official statement.

Explaining the significance of the research, Dr Prosenjit Mondal, IIT Mandi, said, "NAFLD is an independent predictor of insulin resistance and T2DM. However, how NAFLD affects the insulin-releasing pancreatic β-cell function was not fully understood. We aimed at finding the relationship between β-cells failure and the accumulation of liver fat produced from carbohydrates in a process called de novo lipogenesis."

The multi-institutional research team analysed blood samples extracted from fat-fed mice and human NAFLD patients. Both samples had high amounts of a calcium-binding protein termed S100A6. This protein is released by the fatty liver and serves as a communication link between the liver and the pancreas. S100A6 adversely affects the insulin secretion ability of the β-cells, thereby resulting in or exacerbating existing T2DM. At a biochemical level, S100A6 was found to inhibit insulin secretion by activating the receptor for the advanced glycation end product (RAGE) on pancreatic beta-cells, as reported by News 9 live.

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