Next Article in Journal
microRNA-34a as a Therapeutic Agent against Human Cancer
Next Article in Special Issue
MicroRNAs in Nonalcoholic Fatty Liver Disease
Previous Article in Journal
Renin-Angiotensin-Aldosterone System Blockade in Diabetic Nephropathy. Present Evidences
Previous Article in Special Issue
MicroRNA-224 Induces G1/S Checkpoint Release in Liver Cancer
Open AccessReview

MicroRNA Expression Relating to Dietary-Induced Liver Steatosis and NASH

Developmental Epigenetics Group, Liggins Institute, The University of Auckland, 85 Park Road, Grafton, Auckland 1023, New Zealand
Author to whom correspondence should be addressed.
Academic Editor: Rajagopal N. Aravalli
J. Clin. Med. 2015, 4(11), 1938-1950;
Received: 20 August 2015 / Revised: 9 November 2015 / Accepted: 10 November 2015 / Published: 16 November 2015
(This article belongs to the Special Issue MicroRNAs: Novel Biomarkers for Liver Diseases)
PDF [858 KB, uploaded 16 November 2015]


Health issues associated with excessive caloric intake and sedentary lifestyle are driving a modern “epidemic” of liver disease. Initially presenting in the clinic as an excessive accumulation of fat within hepatocyte cells (steatosis), the progression to more severe non-alcoholic steatohepatitis (NASH) in which liver damage and inflammation are overt features, is becoming increasingly common. Often developing as a sequela of obesity, non-alcoholic fatty liver disease (NAFLD) arises in almost one-third of people initially carrying excess hepatic fat and is likely the result of the liver’s limited capacity to cope with the modern-day levels of dietary fatty acids circulating in the blood. While routine imaging can readily assess the presence and level of “extra-hepatic fat”, a proper diagnosis of disease progression to NASH is currently only possible by liver biopsy. A general reluctance to undergo such screening means that the prevalence of NASH is likely to be under reported and, thus, risk assessment for future metabolic syndrome (MetS) markedly compromised. The seemingly inevitable progression to overt insulin resistance that characterizes MetS may in part be the consequence of the body’s attempt to cope with NAFLD by driving systemic insulin sensitivity and, thus, fatty acid breakdown. The potential significance of miRNAs in both physiological homeostasis and pathogenesis is increasingly appreciated and in the liver may contribute specifically to the regulation of lipid pathways and NAFLD progression. As such, they may have utility as molecular indicators for the accurate profiling of both initial risk and disease progression from simple steatosis to NASH, and further to fibrosis/cirrhosis. View Full-Text
Keywords: diet; miRNA; NAFLD; NASH diet; miRNA; NAFLD; NASH

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Zarfeshani, A.; Ngo, S.; Sheppard, A.M. MicroRNA Expression Relating to Dietary-Induced Liver Steatosis and NASH. J. Clin. Med. 2015, 4, 1938-1950.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top