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Updated: Jul 30, 2025
An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
Adipose tissue macrophage-derived exosomal miR-210-5p in modulating insulin sensitivity in rats born small for
Hui Xiong1, Wei Liu1, Jie Song2
1Department of Pediatrics, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Insights
MicroRNA-210-5p delivered by exosomes from adipose tissue macrophages promotes insulin resistance in small for gestational age rats with catch-up growth. Targeting SIDT2 may offer a therapeutic strategy for these children.
Area of Science:
- Endocrinology
- Molecular Biology
- Metabolic Research
Background:
- Insulin resistance is a key factor in the development of children born small for gestational age (SGA) who experience catch-up growth (CUG).
- Adipose tissue macrophages (ATMs) secrete exosomes containing microRNA (miRNA) that influence insulin resistance, but the precise mechanisms are not fully understood.
- This study investigates the role of miR-210-5p in insulin resistance in rats born SGA with CUG.
Purpose of the Study:
- To elucidate the role of miR-210-5p in insulin resistance in rats born SGA with CUG.
- To identify the molecular mechanism by which miR-210-5p contributes to insulin resistance.
- To explore potential therapeutic targets for SGA with CUG.
Main Methods:
- Induction of SGA in rats via dietary restriction.
- Isolation and characterization of exosomes from ATMs using Transmission Electron Microscopy (TEM) and Western blot.
- Confirmation of exosome uptake via PKH-67 staining.
- Quantification of miR-210-5p expression using qRT-PCR.
- Assessment of glucose uptake/output and insulin sensitivity in vivo.
- Validation of the interaction between miR-210-5p and SIDT2 using a dual-luciferase reporter assay.
Main Results:
- Exosomes derived from ATMs of CUG-SGA rats showed significantly higher miR-210-5p expression.
- ATM-derived exosomes effectively delivered miR-210-5p into target cells (adipocytes, myocytes, hepatocytes), exacerbating insulin resistance.
- SIDT2 was identified as a direct target of miR-210-5p, and its restoration reversed miR-210-5p-induced insulin resistance.
- Overexpression of SIDT2 diminished the negative impact of CUG-SGA-ATM-exosomal miR-210-5p on insulin sensitivity.
Conclusions:
- ATM-derived exosomal miR-210-5p promotes insulin resistance in CUG-SGA rats by targeting SIDT2.
- This pathway represents a novel molecular mechanism contributing to insulin resistance in this condition.
- Targeting the miR-210-5p/SIDT2 axis offers a potential therapeutic strategy for children born SGA with CUG.
Background:
Insulin resistance has been implicated in the pathogenesis of children born small for gestational age (SGA) with catch-up growth (CUG). Adipose tissue macrophages (ATMs) regulate insulin resistance by secreting exosomes containing microRNA (miRNA) cargo; however, their pathogenic roles and molecular mechanism are not fully understood. This study aimed to investigate the role of miR-210-5p in rats born SGA with CUG and insulin resistance.
Methods:
The dietary needs of pregnant rats were restricted to ensure the birth of SGA rats. Transmission electron microscopy (TEM) and Western blot analysis were used to identify the exosomes from ATMs of CUG-SGA and adequate-for-gestational-age (AGA) rats. PKH-67 staining was performed to confirm the uptake of exosomes. miR-210-5p expression was measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Glucose uptake and output were detected with glucose uptake and output assays, respectively. Insulin resistance was detected with glucose and insulin tolerance tests in vivo. The interaction between miR-210-5p and SID1 transmembrane family member 2 (SIDT2) was validated with dual-luciferase reporter assay.
Results:
miR-210-5p was observed to be highly expressed in the exosomes derived from the ATMs of CUG-SGA rats. ATM-derived exosomes can serve as vehicles to deliver miR-210-5p into adipocytes, myocytes, and hepatocytes, where it can enhance cellular insulin resistance. SIDT2 was identified as a direct target gene of miR-210-5p. The miR-210-5p-induced insulin resistance was reversed by the restored SIDT2 expression. However, overexpression of SIDT2 abolished the inhibitory effect of CUG-SGA-ATM-exosomal miR-210-5p on insulin sensitivity in vivo.
Conclusions:
ATM-derived exosomal miR-210-5p promoted insulin resistance in CUG-SGA rats by targeting SIDT2, which may act as a new potential therapeutic target for children born SGA with CUG.
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