E-Paper
IIT-Mandi researchers find link between fatty liver disease, Type-2 diabetes
The findings offer new diagnostic and therapeutic tools to control or even reverse fatty-liver-induced diabetes
The researchers at the Indian Institute of Technology, Mandi, found a biochemical relationship 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). The findings also had the potential to offer new therapeutic pathways to control or even reverse fatty liver-induced diabetes.
The findings of the research have been published in the Journal of diabetes.
The paper has been jointly authored by Prosenjit Mondal, associate professor, School of Biosciences and Bioengineering, research scholars Surbhi Dogra, Priya Rawat, P Vineeth Daniel from IIT Mandi, Partha Chakrabarti from CSIR-Indian Institute of Chemical Biology, Kolkata, Debajyoti Das, Sujay K. Maity, Avishek Paul along with Dr Kausik Das, and Dr Souveek Mitra from IPGMER and SSKM Hospital, Kolkata.
Explaining the significance of the research, Mondal, 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.” He said.
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, which is released by the fatty liver and serves as a communication link between the liver and the pancreas.
Protein 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 Advanced Glycation End product (RAGE) on pancreatic beta-cells, said Mondal.
Elaborating on the critical work, Surbhi Dogra, said that another important observation from our research was that “the depletion of S100A6 improves insulin secretion and the regulation of blood glucose in mice.”
This study is important on many counts, she said, adding that at a scientific level, it presents the molecular and cellular events associated with S100A6 secretion in fatty liver, and its adverse impact on β-cell insulin release.
From a practical, diagnostic angle, it shows that elevated levels of S100A6 in the blood may serve as a biomarker to identify risks of T2DM among NAFLD patients, said Dogra.
Mondal said the research was important for India because the prevalence of NAFLD was rapidly increasing in the country and recent surveys show that 40% of Indian adults suffer from it.
