IIT Mandi study finds biochemical link between fatty liver disease, Type 2 Diabetes
IIT Mandi research will help diagnose the risk of diabetes in people with Non-Alcoholic Fatty Liver Disease.
Ishaan Arora | September 6, 2022 | 03:35 PM IST
NEW DELHI: The researchers at the Indian Institute of Technology (IIT) Mandi have discovered the biochemical relationship between fatty liver disease and Type 2 Diabetes Mellitus (T2DM). According to the researchers, the findings will aid in the diagnosis of Diabetes in people with Non-Alcoholic Fatty Liver Disease (NAFLD).
The findings of the research have been published in the Journal of Diabetes. "The paper has been authored by Prosenjit Mondal, Associate Professor, School of Biosciences and Bioengineering, IIT Mandi, along with his scholars Surbhi Dogra, Priya Rawat, P Vineeth Daniel, and In collaboration with Partha Chakrabarti from CSIR-Indian Institute of Chemical Biology, Kolkata, Debajyoti Das, Sujay K. Maity, Avishek Paul along with Kausik Das, and Souveek Mitra from IPGMER and SSKM Hospital, Kolkata," the statement from IIT Mandi said.
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Explaining the research, Mondal said, “Targeting β-cells to improve its function and survival is of utmost importance for diabetes management, on the relevance of this work in devising new therapies for metabolic syndrome diseases such as Type 2 Diabetes and NAFLD."
The researchers first shortlisted the blood samples extracted from fat-fed mice and human NAFLD patients. The sample contained calcium-binding protein termed S100A6 in a very high amount. S100A6 impairs insulin sensitivity in β-cells, resulting in or exacerbating T2DM.
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Given that 40% of Indians currently live with NAFLD, the study's findings were helpful for India. The study helps to remove S100A6 from blood, which can help to maintain β-cell function. In turn, β-cell supports the recovery of RAGE antagonistic molecules in NAFLD patients.
Speaking about the research, Dogra said, “Another important observation from our research was that the depletion of S100A6 improves insulin secretion and the regulation of blood glucose in mice, which suggests that S100A6 contributes to the pathophysiology of diabetes in NAFLD.”
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