SFEBES2019 POSTER PRESENTATIONS Metabolism and Obesity (104 abstracts)
Regulation and role of MiR-125b in β-cells
Grazia Pizza 1 , Rebecca Cheung 1 , Delphine Rolando 1 , Marie-Sophie Nguyen-Tu 1 , Ines Cebola 1 , Pauline Chabosseau 1 , Piero Marchetti 2 , James Shapiro 3 , Lorenzo Piemonti 4 , Kei Sakamoto 5 , David M Smith 6 , Guy A Rutter 1 & Aida Martinez-Sanchez 1
1Imperial College London, London, UK; 2University of Pisa, Pisa, Italy; 3University of Alberta, Edmonton, Canada; 4Vita-Salute San Raffaele, Milan, Italy; 5Nestle Institute of Health Sciences, Lausanne, Swaziland; 6Astrazeneca, Cambridge, UK
MicroRNAs (miRNAs) are small non-coding RNAs that repress protein production post-transcriptionally. MiRNAs play crucial roles in metabolism, endocrine cells development and in processes altered in T2D, such as insulin secretion. MiR-125b controls proliferation, apoptosis and differentiation of various cell types, although its role in β-cells remains unclear. Recent studies show an association between high levels of circulating miR-125b and hyperglycaemia (HbA1c) in prediabetes, T1D and T2D, suggesting this miRNA as a biomarker/contributor to the disease. I aim to determine whether glucose regulates miR-125b expression in β-cells and to understand its function by identifying its gene targets. We found that miR-125b expression is regulated by glucose in both mouse and human islets via AMP-activated protein kinase (AMPK), an important regulator of glucose homeostasis and target for anti-diabetic drugs. A combined analysis of both RNA-Seq and RNA-Immunoprecipitation of the miRNA-induced silencing complex (RIP-Seq) in β-cells overexpressing miR-125b identified dozens of novel miR-125b targets such as M6pr and Mtfp1, involved in enzyme sorting within secretory granules and mitochondrial fission and revealed a role for miR-125b in respiration and cytokine receptor interactions. Thus, miR-125b arises as an important regulator of β-cell function with a potential role in the deleterious effects of hyperglycaemia on β-cells.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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