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Early life programming and the risk of non-alcoholic fatty liver disease

Published online by Cambridge University Press:  23 January 2017

C. Lynch ,
C. S. Chan  and
A. J. Drake
C. Lynch
Affiliation:
Edinburgh Medical School, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK
C. S. Chan
Affiliation:
Edinburgh Medical School, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK
A. J. Drake*
Affiliation:
University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK
*
*Address for correspondence: A. J. Drake, University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, 47, Little France Crescent, Edinburgh EH16 4TJ, UK. (Email [email protected])
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Abstract

Non-alcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance, type 2 diabetes and cardiovascular disease and can be considered the hepatic manifestation of the metabolic syndrome. NAFLD represents a spectrum of disease, from the relatively benign simple steatosis to the more serious non-alcoholic steatohepatitis, which can progress to liver cirrhosis, hepatocellular carcinoma and end-stage liver failure, necessitating liver transplantation. Although the increasing prevalence of NAFLD in developed countries has substantial implications for public health, many of the precise mechanisms accounting for the development and progression of NAFLD are unclear. The environment in early life is an important determinant of cardiovascular disease risk in later life and studies suggest this also extends to NAFLD. Here we review data from animal models and human studies which suggest that fetal and early life exposure to maternal under- and overnutrition, excess glucocorticoids and environmental pollutants may confer an increased susceptibility to NAFLD development and progression in offspring and that such effects may be sex-specific. We also consider studies aimed at identifying potential dietary and pharmacological interventions aimed at reducing this risk. We suggest that further human epidemiological studies are needed to ensure that data from animal models are relevant to human health.

Keywords

early life programmingglucocorticoidsmaternal nutritionnon-alcoholic fatty liver disease
Type
Review
Information
Journal of Developmental Origins of Health and Disease , Volume 8 , Issue 3 , June 2017 , pp. 263 - 272
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2017 

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Footnotes

†

These authors contributed equally to this work.

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