Metabolic Programming of Hepatic Organ Function—2nd Edition

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (31 July 2025) | Viewed by 1101

Special Issue Editor


E-Mail
Guest Editor
Department of Gastroenterology and Hepatology, Faculty of Medicine and University Hospital Cologne, University of Cologne, 50937 Cologne, Germany
Interests: hepatology; MASLD; MASH; liver cirrhosis; hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

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. A 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) may 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 they are more susceptible to cardiometabolic disorders such as obesity, insulin resistance, hypertension, dyslipidemia, or metabolic-associated steatotic 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.

The second edition of this Special Issue of Metabolites, which follows the previous edition (https://www.mdpi.com/journal/metabolites/special_issues/Y4O8G4S97Y), continues aiming 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, diagnostic, and treatment approaches.

The topics that this Special Issue will cover include, among others, metabolic dysfunction-associated steatotic liver disease (MASLD), 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
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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 2700 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.

Keywords

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

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 2576 KB  
Article
The Hidden Players of the Fecal Metabolome: Metabolic Dysregulation Beyond SCFAs Under a High-Fat Diet
by María Martín-Grau, Pilar Casanova, José Manuel Morales, Vannina González Marrachelli and Daniel Monleón
Metabolites 2025, 15(10), 660; https://doi.org/10.3390/metabo15100660 - 7 Oct 2025
Viewed by 682
Abstract
Background/Objectives: The interplay between host metabolism and gut microbiota is central to the pathophysiology of metabolic diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). In this study, we investigated the underexplored fecal host–microbiota co-metabolism profile of male and female Wistar rats after 21 [...] Read more.
Background/Objectives: The interplay between host metabolism and gut microbiota is central to the pathophysiology of metabolic diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). In this study, we investigated the underexplored fecal host–microbiota co-metabolism profile of male and female Wistar rats after 21 weeks of high-fat diet (HFD), a model previously validated for early MASLD. Methods: Using 1H-NMR spectroscopy, we detected and quantified metabolites in fecal samples associated with hepatic metabolism beyond short-chain fatty acids (SCFAs), such as energy-related metabolites, amino acid turnover, branched-chain amino acid (BCAA) catabolism, and microbial fermentation. Results: Distinct metabolic signatures were identified according to diet and sex, and statistical analysis was performed. Notably, alterations were observed in bile acids (BAs) such as cholate and glycocholate, suggesting disruptions in enterohepatic circulation. The presence of fucose, a sugar linked to liver pathology, was also elevated. Energy-related metabolites indicated a shift from lactate production to increased acetoacetate and malonate levels, implying redirection of pyruvate metabolism and inhibition of the TCA cycle. BCAA derivatives such as 3-methyl-2-oxovalerate and 3-aminoisobutyrate were altered, supporting earlier findings on disrupted amino acid metabolism under HFD conditions. Furthermore, microbial metabolites including methanol and ethanol showed group-specific differences, suggesting shifts in microbial activity. Conclusions: These findings complement previous longitudinal data and provide a functional interpretation of newly identified metabolites. These metabolites, previously unreported, are now functionally contextualized and linked to hepatic and microbial dysregulation, offering novel biological insights into early MASLD mechanisms. Full article
(This article belongs to the Special Issue Metabolic Programming of Hepatic Organ Function—2nd Edition)
Show Figures

Graphical abstract

Back to TopTop