Obesity is a risk factor for pancreatic β-cell dysfunction and subsequent development of type 2 diabetes. In this process, it is believed that the obese condition generates increased stress on the β-cell, leading to progressive β-cell failure and dysregulated blood glucose levels. However, it is known that a subset of the obese population is still able to maintain β-cell function and euglycemia. Despite intensive studies over the past two decades, the differences in β-cell function that distinguishes this subset from those that develop diabetes remain unclear. 

Pancreatic β-cell function is crucial for systemic glucose metabolism and is regulated in both a cell-autonomous manner and also via communication with other tissues and organs. For example, recent works indicate that unidentified liver-derived humoral factor(s) impact on β-cell mass and insulin secretion capacity. Of note, recent evidence indicates that small RNAs exist in circulation and that these RNAs may act like hormonal factors involved in integrative organ crosstalk. We have investigated the role of circulating small RNAs in integrative organ crosstalk between liver and pancreatic β-cells.