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MicroRNAs

MicroRNAs

MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...

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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

A decrease in hepatic microRNA-9 expression impairs gluconeogenesis by targeting FOXO1 in obese mice.

Caifeng Yan^1,2, Jinfeng Chen³, Min Li²

¹Department of Endocrinology, Clinical Medical College of Yangzhou University, Yangzhou, China.

|March 23, 2016

Summary

This summary is machine-generated.

Reduced microRNA-9 (miR-9) expression in obese mice is linked to increased gluconeogenesis. Restoring miR-9 improves insulin sensitivity and inhibits hepatic glucose production, highlighting its role in metabolic regulation.

Keywords:

DNA methylation FOXO1 Insulin resistance MicroRNA-9

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Area of Science:

Metabolic regulation
Molecular biology
Diabetes research

Background:

MicroRNA-9 (miR-9) is known to regulate pancreatic beta cell function.
The specific role of miR-9 in hepatic gluconeogenesis remains largely uncharacterized.
Understanding miR-9's function in glucose metabolism is crucial for metabolic disease research.

Purpose of the Study:

To investigate the role of microRNA-9 (miR-9) in hepatic glucose production (HGP).
To elucidate the regulatory mechanisms of miR-9 in the context of obesity and gluconeogenesis.
To determine the impact of miR-9 modulation on glucose homeostasis and insulin sensitivity.

Main Methods:

Assessed miR-9 expression and promoter methylation in livers of diet-induced obese and genetic obese mouse models.
Utilized methylation-specific PCR, ChIP, and quantitative real-time PCR to analyze miR-9 promoter regulation by DNA methyltransferases (DNMTs).
Evaluated HGP in vitro and in vivo, alongside glucose tolerance, insulin tolerance, and pyruvate tolerance tests.

Main Results:

Obese mice exhibited reduced miR-9 expression and increased miR-9-3 promoter hypermethylation.
DNA methyltransferase 1 (DNMT1) binding to the miR-9-3 promoter was elevated in obese hepatocytes, suppressing miR-9 expression.
Overexpression of hepatic miR-9 improved insulin sensitivity and inhibited HGP in obese mice, while miR-9 deletion increased blood glucose levels.
Silencing forkhead box O1 (FOXO1) reversed the effects of miR-9 deletion on gluconeogenesis.

Conclusions:

Decreased miR-9 expression contributes to dysregulated gluconeogenesis in obese mice.
miR-9 plays a critical role in regulating hepatic glucose production and insulin sensitivity.
Targeting miR-9 may represent a therapeutic strategy for managing metabolic disorders associated with hyperglycemia.