# Regulatory microRNAs in Brown, Brite and White Adipose Tissue

## TL;DR

This paper reviews how specific microRNAs regulate different types of fat tissue, which could lead to new treatments for obesity and related diseases.

## Contribution

The paper provides a comprehensive and updated overview of regulatory miRNAs in brown, brite, and white adipose tissues.

## Key findings

- Certain miRNAs like MiR-328 and MiR-378 promote brown adipogenesis.
- Other miRNAs such as MiR-34a and MiR-133 inhibit brown adipogenesis.
- Understanding miRNA roles in adipose tissues may lead to novel therapies for obesity and diabetes.

## Abstract

MicroRNAs (miRNAs) constitute a class of short noncoding RNAs which regulate gene expression by targeting messenger RNA, inducing translational repression and messenger RNA degradation. This regulation of gene expression by miRNAs in adipose tissue (AT) can impact on the regulation of metabolism and energy homeostasis, particularly considering the different types of adipocytes which exist in mammals, i.e., white adipocytes (white AT; WAT), brown adipocytes (brown AT; BAT), and inducible brown adipocytes in WAT (beige or brite or brown-in-white adipocytes). Indeed, an increasing number of miRNAs has been identified to regulate key signaling pathways of adipogenesis in BAT, brite AT, and WAT by acting on transcription factors that promote or inhibit adipocyte differentiation. For example, MiR-328, MiR-378, MiR-30b/c, MiR-455, MiR-32, and MiR-193b-365 activate brown adipogenesis, whereas MiR-34a, MiR-133, MiR-155, and MiR-27b are brown adipogenesis inhibitors. Given that WAT mainly stores energy as lipids, whilst BAT mainly dissipates energy as heat, clarifying the effects of miRNAs in different types of AT has recently attracted significant research interest, aiming to also develop novel miRNA-based therapies against obesity, diabetes, and other obesity-related diseases. Therefore, this review presents an up-to-date comprehensive overview of the role of key regulatory miRNAs in BAT, brite AT, and WAT.