The destiny of glucose from a microRNA perspective
- 1URT GDD, Istituto per l'Endocrinologia e l'Oncologia Gaetano Salvatore (CNR), Italy
Glucose serves as a primary, and for some tissues the unique, fuel source in order to generate and maintain the biological functions. Hyperglycemia is a hallmark of type 2 diabetes and is the direct consequence of perturbations in the glucose homeostasis. Insulin resistance, referred to as a reduced response of target tissues to the hormone, contributes to the development of hyperglycemia.
The molecular mechanisms responsible for the altered glucose homeostasis are numerous and not completely understood. microRNAs are now recognized as regulators of the lipid and glucose metabolism and are involved in the onset of metabolic diseases. Indeed, these small non-coding RNA molecules operate in the RNA silencing and post-transcriptional regulation of gene expression and may modulate the levels of kinases and enzymes in the glucose metabolism.
Therefore, a better characterization of the function of microRNAs and a deeper understanding of their role in disease may represent a fundamental step towards innovative treatments addressing the causes, not only the symptoms, of hyperglycemia, using approaches aimed at restoring either microRNAs or their specific targets.
In this review, we outline the current understanding regarding the impact of microRNAs in the glucose metabolism and highlight the need for further research focused on altered key kinases and enzymes in metabolic diseases.
Keywords: glucose metabolism, insulin signaling, Insulin Resistance, MicroRNAs, post-transcriptional regulation
Received: 15 Dec 2017;
Accepted: 05 Feb 2018.
Edited by:Antonio Brunetti, Magna Græcia University, Italy
Reviewed by:Sinan Tanyolac, Istanbul University, Turkey
Rodolfo Iuliano, Magna Græcia University, Italy
Copyright: © 2018 Mirra, Nigro, Prevenzano, Leone, Raciti, Formisano, Beguinot and Miele. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Claudia Miele, Istituto per l'Endocrinologia e l'Oncologia Gaetano Salvatore (CNR), URT GDD, Via Pansini 5, Naples, 80131, Italy, email@example.com