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An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes
Published on: April 26, 2019
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Stress-activated miR-21/miR-21* in hepatocytes promotes lipid and glucose metabolic disorders associated with
Nicolas Calo1, Pierluigi Ramadori1, Cyril Sobolewski1
1Department of Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Gut
|May 26, 2016
Summary
MicroRNA-21 (miR-21) deficiency improves glucose intolerance and fatty liver in diet-induced obesity. This suggests miR-21 is a potential therapeutic target for metabolic liver disease and syndrome.
Area of Science:
- Molecular Biology
- Hepatology
- Metabolic Disorders
Background:
- MicroRNA-21 (miR-21) is upregulated in liver cancer and steatosis.
- Its role in metabolic liver disorders and progression to cancer is unknown.
Purpose of the Study:
- Investigate the role of miR-21/miR-21* in early metabolic liver disorders.
- Determine the impact of miR-21/miR-21* on diet-induced obesity (DIO).
Main Methods:
- Generated constitutive and liver-specific miR-21/miR-21* knockout mice.
- Fed mice a high-fat diet (HFD) to induce obesity.
- Analyzed lipid and glucose metabolism, serum, and liver tissue.
Main Results:
- miR-21/miR-21* deletion improved glucose intolerance, steatosis, and adiposity in HFD-fed mice.
- Liver-specific deletion of miR-21/miR-21* yielded similar metabolic improvements.
- Hepatocyte miR-21/miR-21* deficiency enhanced insulin sensitivity and modulated key metabolic transcription factors.
Conclusions:
- Hepatic miR-21/miR-21* deficiency prevents metabolic dysfunction in diet-induced obesity.
- miR-21/miR-21* is a potential therapeutic target for non-alcoholic fatty liver disease and metabolic syndrome.
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