Written By: Debjani Arora | Updated : August 31, 2018 2:55 PM IST
Image credits by: Insulin can boost immunity too. © Shutterstock
Till date we have been talking about insulin, a peptide hormone produce by the beta cells of the pancreatic islets with regards to diabetes and high blood glucose levels. However recent studies show that the function of insulin is not restricted to glucose metabolism and dissemination. The Toronto General Hospital Research Institute (TGHRI) scientists have identified a specific insulin signalling pathway that, when activated, revs up the response of T cells in the immune system to divide rapidly and secrete cytokines, chemical messenger proteins that activate the rest of the immune system.
This was definitely a lesser known fact about insulin. Any method that can trigger a fast and efficient immune response protects us from life-threatening infections and diseases while a slow, sluggish and ineffective immune system can cause infections and microbes to spread and lead to diseases to spread. Assistant Professor Dr Dan Winer one of the authors of the study informed the media that they have identified one of metabolism's most popular hormones, specifically the insulin signalling pathway, as a novel 'co-stimulatory' driver of immune system function.
Although much work has been done on the role of insulin in organs such as the liver, muscle and in fat to understand the regulation of glucose or blood sugar and how the body metabolises or turns it into energy, little is known about how insulin impacts the immune system.
The goal of this research was to study how insulin regulates T cell function and what causes T cells to stop responding to insulin, Dr Tsai said, adding that T cells were chosen because they play a pivotal role in self-defense against infections. Using genetically engineered mice, the research team designed mice with T cells that did not have an insulin receptor on them, mimicking insulin resistance. They then observed what happened to the T cells in the mice under different stressors, such as the H1N1 flu virus.
Without the added boost or kickstart provided by the insulin receptor to help "re-energize" the T cells to mount an effective immune response, the T cells failed to destroy viruses such as H1N1 influenza. The full findings are present in the journal Cell Metabolism.
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