Dear Colleagues,

The liver acts as the central regulator of energy homeostasis by orchestrating numerous metabolic processes, e.g., glycolysis, gluconeogenesis, and fatty acid metabolism. Disruption of liver development and maturation as a result of metabolic imbalance early in life may have long-lasting adverse metabolic consequences, rendering the liver more susceptible to chronic diseases in later life.

Accumulating clinical and experimental evidence demonstrates that detrimental early-life risk factors (e.g., maternal obesity) cause an altered genetic, hormonal, and metabolic micro-environment for the developing fetus and thereby adversely influence fetal growth and organ development. For example, infants of obese mothers are at an increased risk for poor neonatal outcomes, including congenital abnormalities, and are more susceptible to cardiometabolic disorders such as obesity, insulin resistance, hypertension, dyslipidemia later, or non-alcoholic fatty liver disease later in life. Experimental studies support the notion that the intrauterine and early-life metabolic environment interferes with developmental processes and thereby determines organ structure, function, and susceptibility to diseases in the offspring. This condition has been coined as the concept of developmental origins of health and diseases (DOHaD), also known as the fetal programming hypothesis.

While increasing evidence suggests that there is also a metabolic programming of hepatic organ function, the underlying mechanisms remain poorly understood.

This Special Issue aims to feature insights into ‘early-life‘ mechanisms involved in the development of hepatic diseases, since a better understanding of these mechanisms could provide new strategies for effective prevention, diagnostics, and treatment. 

The topics that this Special Issue will cover include, among others, metabolic dysfunction-associated fatty liver disease (MAFLD), non-alcoholic fatty liver disease (NAFLD), genetic and epigenetic regulation of liver development, novel diagnostic and prognostic biomarkers, metabolomics, liver crosstalk with other tissues/organs such as adipose tissue or gut, immunometabolism, neuroendocrine mechanisms, hepatocyte-immune cell crosstalk, and developmental programming of glucose and the lipid metabolism.

Studies may use interventions such as dietary approaches or pharmacological treatment and -omics approaches. Both basic and clinical research are welcome.

This Special Issue will publish high-quality original research articles and review articles related to this issue, inspired by, but not limited to the aspects mentioned above.

Dr. Philipp Kasper
Dr. German Perdomo
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• metabolism
• liver
• early-life environment
• developmental programming
• epigenetics
• metabolic syndrome
• obesity
• metabolic-dysfunction-associated fatty liver disease