MiR‐184 expression is regulated by AMPK in pancreatic islets

What is it about?

Diabetes mellitus is a disease that affects 8% of the world population. Central to the development of type 2 diabetes is the failure of the pancreatic β-cell that is normally responsible for insulin secretion in response to high blood glucose. AMP-activated protein kinase is an enzyme that contributes to the control of β-cell function that has been suggested as a possible target for certain anti-diabetic drugs. Nevertheless, it is not well understood how this enzyme works in β-cells. MicroRNAs (miRNAs) are tiny molecules inside cells that regulate the genes that are required for a cell to function normally. β-cells need miRNAs to function properly thus alteration of miRNAs leads to diabetes. Our group has previously generated a mouse model that lacks AMPK in their β-cells. This caused several functional defects and a strong alteration in gene expression. We hypothesized that miRNAs might be involved in these defects. Here we demonstrate that β-cells lacking AMPK contain abnormal levels of several miRNAs which are predicted to affect the function of these cells. One of the identified miRNAs, miR-184, is necessary for the adequate growth of these cells and is controlled by ambient glucose concentrations (that is, available energy). We demonstrate that AMPK is essential for this control and we provide, for the first time, a link between the energy status of the β-cells, AMPK and miRNAs important for β-cell function.

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