Downregulation of Exosomal hsa-miR-551b-3p in Obesity and Its Link to Type 2 Diabetes Mellitus

Author:

Dracheva Kseniia V.12ORCID,Pobozheva Irina A.12,Anisimova Kristina A.3,Balandov Stanislav G.3,Grunina Maria N.1ORCID,Hamid Zarina M.3,Vasilevsky Dmitriy I.3,Pchelina Sofya N.12,Miroshnikova Valentina V.12ORCID

Affiliation:

1. Petersburg Nuclear Physics Institute Named by B.P. Konstantinov of National Research Centre “Kurchatov Institute”, 188300 Gatchina, Russia

2. Department of Molecular-Genetic and Nanobiological Technologies, Scientific Research Center, Pavlov First Saint-Petersburg State Medical University, 197022 Saint Petersburg, Russia

3. Center for Surgical Treatment of Obesity and Metabolic Disorders, Pavlov First Saint-Petersburg State Medical University, 197022 Saint Petersburg, Russia

Abstract

Obesity is a significant risk factor for the development of type 2 diabetes mellitus (T2DM). Adipose tissue dysfunction can affect the pool of circulating exosomal miRNAs, driving concomitant disease in obesity. These exosomal miRNAs can reflect adipose tissue functionality, thus serving as prognostic biomarkers for disease monitoring in case of T2DM. In the present study, we conducted NanoString microRNA profiling of extracellular vesicles (EVs) secreted by adipose tissue of obese patients (body mass index (BMI) > 35) without T2DM and nonobese individuals (BMI < 30) as a control group. Functional and pathway enrichment analysis showed that miRNAs associated with obesity in this study were implicated in insulin signaling and insulin resistance biological pathways. Further, these microRNAs were screened in serum EVs in the following groups: (1) obese patients with T2DM, (2) obese patients without T2DM, and (3) nonobese individuals as a control group. has-miR-551b-3p was shown to be downregulated in adipose tissue EVs, as well as in serum EVs, of patients with obesity without T2DM. At the same time, the serum exosomal hsa-miR-551b-3p content was significantly higher in obese patients with T2DM when compared with obese patients without T2DM and may be a potential biomarker of T2DM development in obesity.

Funder

Russian Science Foundation

Publisher

MDPI AG

Subject

Genetics,Molecular Biology,Biochemistry

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