Mini organs in the pancreas called pancreatic islets are home to beta cells. These beta cells synthesise and secrete insulin, a hormone that regulates blood glucose levels.
In pre-diabetic patients, insulin resistance begins when cells in the muscles, body fat and liver start ignoring the signals sent by insulin to transfer glucose from the bloodstream into cells. To maintain regular blood glucose levels, the beta cells compensate for the reduced sensitivity by boosting insulin secretion in a process that is supported by an increase in the mass and number of beta cells called islet remodelling.
Looking for novel approaches to slow down the progression of diabetes, Asst Prof Yusuf Ali of NTU’s Lee Kong Chian School of Medicine, together with scientists from NTU’s School of Biological Sciences and researchers in Germany and Sweden, investigated the extent to which a particular cell type—islet resident macrophages—contributes to pancreatic remodelling.
Using diabetic mice engineered to lack macrophages, and by designing in vivo experiments where macrophages are specifically depleted from pancreatic islets, the researchers observed significantly reduced pancreatic remodelling and insulin secretion. Mice lacking macrophages in islets rapidly developed diabetes.
Understanding the role played by islet macrophages in pancreatic remodelling may be useful in finding treatments that halt or slow down the transition from pre-diabetes to full diabetes, the researchers say.
The study “Islet macrophages are associated with islet vascular remodelling and compensatory hyperinsulinemia during diabetes” was published in American Journal of Physiology–Endocrinology and Metabolism (2019), DOI: 10.1152/ajpendo.00248.2019.