Endocrine Abstracts

Background and aim: Obesity (Ob) is tightly associated with metabolic diseases such as type 2 diabetes (DT2) andinsulin resistance (IR). Furthermore, obesity has been identified as one of the primary causes of mood disorders (MDs) including depression. Several studies have demonstrated the link between Ob, adiposity, neuroinflammation and MDs. The Brain-Derived Neurotrophic Factor (BDNF) and its regulator, the non-coding RNA BDNF antisense RNA (BDNFas), play an important role on the depression pathophysiology and therapeutic antidepressive mechanisms. However, the relation between BDNF and BDNFas, adipose tissue (AT) functionality and Ob has not yet been well defined. Preliminary, in silicoanalysis carried out by our grouphave shown that BDNF and BDNFas are validated target genes of miR-10a, miR-210, miR-182 and miR-27b. Thus, the aim of our study was to analyze the expression of these miRNAs, BDNFand BDNFas in human AT in Ob.

Materials and methods: miR-10a, miR-182, miR-210, miR-27, BDNF and BDNFas expression levels were measured by real-time qPCR from subcutaneous (SAT) and visceral (VAT) adipose tissue of normoweight subjects (NW, n = 9) and metabolically healthy morbid obese (MHO, n = 9).

Results: In this study, we observed that VAT miR-10a, miR-27b and BDNFas expression increased significantly in metabolically healthy obese subjects compared to NW individuals, while no significant changes were observed in miR-210 or BDNF expression. The expression levels of miR-10a, miR-27b, miR-210, BDNF and BDNFas in SAT were also higher in obese subjects compared to NW individuals. The correlative analysis has shown that the expression of miR-182 is positively correlated with BDNFas expression in VAT (r = 0.492; P ˂ 0.05) whereas miR-210 expression is positively correlated with BDNF expression in SAT (r = 0.5089; P ˂ 0.05).

Conclusion: Our results uncover new putative regulatory pathways involving miR-10a, miR-210, miR-182 and miR-27b in the control of the neuroinflammatory genes BDNF and BDNFas during obesity, and pave the way for future studies on the mechanisms which link obesity and mood disorders.

This work was supported by grants from the Spanish Ministry of Health (FIS), PI18/00785 and Miguel Servet II’ [CPII13/00041], and from Consejería de Innovación co-funded by Fondo Europeo de Desarrollo Regional (FEDER) (CTS-7895), and from Consejería de salud co-funded by Fondo Europeo de Desarrollo Regional (FEDER) [PI-0092-2017].

S.L. was a recipient of a post-doctoral grant Plan Propio UMA (2019/REGSED-6636) from the University of Malaga.

M.C.P. was a recipient of a post-doctoral grant Juan de la Cierva Formación (FJCI-2017-32194) from the Ministerio de Ciencia, Innovación y Universidades (Spain).