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Metabolomics to Understand Diet-Related Metabolic Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrigenetics and Nutrigenomics".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 1469

Special Issue Editor


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Guest Editor
CarMeN Laboratory, UMR INSERM U1060/INRAE U1397, Université Claude Bernard Lyon 1, Université de Lyon, 69310 Pierre-Bénite, France
Interests: adaptation and alteration of the metabolome; mitochondrial level to the whole organism; significance of the exometabolome, metabolic diseases (obesity and cancer); precision nutrition

Special Issue Information

Dear Colleagues,

Diet-related metabolic diseases pose significant public health challenges. Metabolomics serves as a powerful tool to decipher the intricate relationship between dietary factors and metabolic health. Furthermore, this approach permits the elucidation of targets for optimized disease prevention and treatment. Metabolomics studies have already paved the way for precision medicine and demonstrate potential for precision nutrition in the context of diet-based pathologies. 

This Special Issue seeks to underscore the methodological advancements that highlight the suitability of metabolomics for exploring the relationship between diet and key pathologies (diabetes, neuronal disorders and cardiovascular diseases) and also investigate the benefits of certain diets (Mediterranean diet and ketogenic diet). Authors are encouraged to focus on the study of biofluids to determine the endometabolome (serum, tissue or cell extract) as well as exometabolome (cell culture supernatant or urine) from a diverse range of models that include in vitro models, animals, and patient cohorts. This Special Issue especially invites contributions that employ a quantitative metabolomics strategy.

Dr. Baptiste Panthu
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • diet-related metabolic diseases
  • Metabolomics
  • dietary factors
  • metabolic health
  • precision nutrition
  • precision medicine

Published Papers (1 paper)

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Research

17 pages, 2635 KiB  
Article
Human Pancreatic Islets React to Glucolipotoxicity by Secreting Pyruvate and Citrate
by Johan Perrier, Margaux Nawrot, Anne-Marie Madec, Karim Chikh, Marie-Agnès Chauvin, Christian Damblon, Julia Sabatier, Charles H. Thivolet, Jennifer Rieusset, Gilles J. P. Rautureau and Baptiste Panthu
Nutrients 2023, 15(22), 4791; https://doi.org/10.3390/nu15224791 - 15 Nov 2023
Cited by 1 | Viewed by 1211
Abstract
Progressive decline in pancreatic beta-cell function is central to the pathogenesis of type 2 diabetes (T2D). Here, we explore the relationship between the beta cell and its nutritional environment, asking how an excess of energy substrate leads to altered energy production and subsequent [...] Read more.
Progressive decline in pancreatic beta-cell function is central to the pathogenesis of type 2 diabetes (T2D). Here, we explore the relationship between the beta cell and its nutritional environment, asking how an excess of energy substrate leads to altered energy production and subsequent insulin secretion. Alterations in intracellular metabolic homeostasis are key markers of islets with T2D, but changes in cellular metabolite exchanges with their environment remain unknown. We answered this question using nuclear magnetic resonance-based quantitative metabolomics and evaluated the consumption or secretion of 31 extracellular metabolites from healthy and T2D human islets. Islets were also cultured under high levels of glucose and/or palmitate to induce gluco-, lipo-, and glucolipotoxicity. Biochemical analyses revealed drastic alterations in the pyruvate and citrate pathways, which appear to be associated with mitochondrial oxoglutarate dehydrogenase (OGDH) downregulation. We repeated these manipulations on the rat insulinoma-derived beta-pancreatic cell line (INS-1E). Our results highlight an OGDH downregulation with a clear effect on the pyruvate and citrate pathways. However, citrate is directed to lipogenesis in the INS-1E cells instead of being secreted as in human islets. Our results demonstrate the ability of metabolomic approaches performed on culture media to easily discriminate T2D from healthy and functional islets. Full article
(This article belongs to the Special Issue Metabolomics to Understand Diet-Related Metabolic Diseases)
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