In recent years, microRNAs, a class of small, evolutionarily conserved, noncoding RNAs, have emerged as key regulators of processes in pancreatic islets, including β-cell function, proliferation and survival. Previous studies have found one of these, miR-132, to be highly expressed in the pancreatic islets of several obesity models, resulting in enhanced glucose-stimulated insulin secretion in vitro.

Mulder and colleagues therefore explored whether over-expression of miR-132 could have a potential therapeutic benefit in insulin-resistant conditions. They injected viral constructs containing miR-132 into the pancreatic duct, leading to its expression specifically in β-cells of pancreatic islets. They found that increasing miR-132 levels in β-cells improved glucose tolerance in mice fed a high-fat diet. Furthermore, in line with previous findings, islets isolated from these mice also secreted more insulin in response to glucose.

Their findings highlight the potential beneficial effects of modulating miRNAs to improve β-cell function.

Read the full article in Journal of Endocrinology doi:10.1530/JOE-18-0287