Emerging roles of non‐coding RNAs in pancreatic β‐cell function and dysfunction

C Guay, C Jacovetti, V Nesca, A Motterle… - Diabetes, Obesity …, 2012 - Wiley Online Library
C Guay, C Jacovetti, V Nesca, A Motterle, K Tugay, R Regazzi
Diabetes, Obesity and Metabolism, 2012Wiley Online Library
Pancreatic β‐cells play a central role in glucose homeostasis by tightly regulating insulin
release according to the organism's demand. Impairment of β‐cell function due to hostile
environment, such as hyperglycaemia and hyperlipidaemia, or due to autoimmune
destruction of β‐cells, results in diabetes onset. Both environmental factors and genetic
predisposition are known to be involved in the development of the disease, but the exact
mechanisms leading to β‐cell dysfunction and death remain to be characterized. Non …
Abstract
Pancreatic β‐cells play a central role in glucose homeostasis by tightly regulating insulin release according to the organism's demand. Impairment of β‐cell function due to hostile environment, such as hyperglycaemia and hyperlipidaemia, or due to autoimmune destruction of β‐cells, results in diabetes onset. Both environmental factors and genetic predisposition are known to be involved in the development of the disease, but the exact mechanisms leading to β‐cell dysfunction and death remain to be characterized. Non‐coding RNA molecules, such as microRNAs (miRNAs), have been suggested to be necessary for proper β‐cell development and function. The present review aims at summarizing the most recent findings about the role of non‐coding RNAs in the control of β‐cell functions and their involvement in diabetes. We will also provide a perspective view of the future research directions in the field of non‐coding RNAs. In particular, we will discuss the implications for diabetes research of the discovery of a new communication mechanism based on cell‐to‐cell miRNA transfer. Moreover, we will highlight the emerging interconnections between miRNAs and epigenetics and the possible role of long non‐coding RNAs in the control of β‐cell activities.
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