Metabolites

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Special Issue Editors

Dr. Julien H. Park

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Guest Editor

Klinik für Kinder- und Jugendmedizin – Allgemeine Pädiatrie, Universitätsklinikum Münster, Münster, Germany
Interests: glycosylation; glycomics; biomarkers; inborn errors of metabolism

Prof. Dr. Thorsten Marquardt

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Guest Editor

Klinik für Kinder- und Jugendmedizin – Allgemeine Pädiatrie, Universitätsklinikum Münster, Münster, Germany
Interests: glycosylation; biomarkers; inborn errors of metabolism; rare diseases

Special Issue Information

Dear Colleagues,

Glycosylation is a key part of translational processing, with an enormous impact on protein function in virtually all metabolic processes. Since their discovery by Prof. Jaeken in the early 1980s, congenital disorders of glycosylation (CDGs) have continued to be an ever-growing and oftentimes challenging subentity among inborn errors of metabolism. From the beginning, diagnosis relied on the analysis of glycosylation in blood samples, starting with analysis of selected biomarkers such as transferrin.

Recent years have seen the advent of more comprehensive, mass-spectrometry-based methods of analysis leading to increased diagnostic yield and the identification of more subtle changes in glycosylation that are missed by conventional methods of analysis. This glycome profiling approach continues to revolutionise the diagnosis of glycosylation disorders.

In this Special Issue of Metabolites, we will explore the impact of these novel analytical methods on the diagnosis and management of disorders associated with altered glycosylation. A special focus will be on novel therapeutic approaches and the potential impact of improved monitoring on the implementation of such therapies. Furthermore, we will explore recent additions to the spectrum of glycosylation disorders ranging from recently discovered disturbances in glycosylation pathways to abnormal glycosylation as a secondary phenomenon in diseases of intracellular homeostasis.

Dr. Julien H. Park
Prof. Dr. Thorsten Marquardt
Guest Editors

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. 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

glycosylation
congenital disorders of glycosylation
glycome
mass spectrometry
biomarkers

Published Papers (2 papers)

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Research

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14 pages, 3099 KiB

Open AccessArticle

Mannose Receptor Deficiency Impacts Bone Marrow and Circulating Immune Cells during High Fat Diet Induced Obesity

by Jasmine Nour, Annalisa Moregola, Monika Svecla, Lorenzo Da Dalt, Rossella Bellini, Olivier Neyrolles, Gian Paolo Fadini, Yoann Rombouts, Mattia Albiero, Fabrizia Bonacina and Giuseppe Danilo Norata

Metabolites 2022, 12(12), 1205; https://doi.org/10.3390/metabo12121205 - 1 Dec 2022

Cited by 11 | Viewed by 2043

Abstract

The mannose receptor C-type 1 (Mrc1) is a C-type lectin receptor expressed on the immune cells and sinusoidal endothelial cells (ECs) of several tissues, including the bone marrow (BM). Parallel to systemic metabolic alterations and hematopoietic cell proliferation, high-fat diet (HFD) feeding increases the expression of Mrc1 in sinusoidal ECs, thus calling for the investigation of its role in bone marrow cell reprogramming and the metabolic profile during obesity. Mrc1^−/− mice and wild-type (WT) littermates were fed an HFD (45% Kcal/diet) for 20 weeks. Weight gain was monitored during the diet regimen and glucose and insulin tolerance were assessed. Extensive flow cytometry profiling, histological, and proteomic analyses were performed. After HFD feeding, Mrc1^−/− mice presented impaired medullary hematopoiesis with reduced myeloid progenitors and mature cells in parallel with an increase in BM adipocytes compared to controls. Accordingly, circulating levels of neutrophils and pro-inflammatory monocytes decreased in Mrc1^−/− mice together with reduced infiltration of macrophages in the visceral adipose tissue and the liver compared to controls. Liver histological profiling coupled with untargeted proteomic analysis revealed that Mrc1^−/− mice presented decreased liver steatosis and the downregulation of proteins belonging to pathways involved in liver dysfunction. This profile was reflected by improved glucose and insulin response and reduced weight gain during HFD feeding in Mrc1^−/− mice compared to controls. Our data show that during HFD feeding, mannose receptor deficiency impacts BM and circulating immune cell subsets, which is associated with reduced systemic inflammation and resistance to obesity development. Full article

(This article belongs to the Special Issue Glycosylation in the Human Metabolism of Congenital Metabolic Diseases)

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Review

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16 pages, 1751 KiB

Open AccessReview

O-GlcNAc Modification and Its Role in Diabetic Retinopathy

by Chengzhi Liu, Wenkang Dong, Jun Li, Ying Kong and Xiang Ren

Metabolites 2022, 12(8), 725; https://doi.org/10.3390/metabo12080725 - 5 Aug 2022

Cited by 7 | Viewed by 2516

Abstract

Diabetic retinopathy (DR) is a leading complication in type 1 and type 2 diabetes and has emerged as a significant health problem. Currently, there are no effective therapeutic strategies owing to its inconspicuous early lesions and complex pathological mechanisms. Therefore, the mechanism of molecular pathogenesis requires further elucidation to identify potential targets that can aid in the prevention of DR. As a type of protein translational modification, O-linked β-N-acetylglucosamine (O-GlcNAc) modification is involved in many diseases, and increasing evidence suggests that dysregulated O-GlcNAc modification is associated with DR. The present review discusses O-GlcNAc modification and its molecular mechanisms involved in DR. O-GlcNAc modification might represent a novel alternative therapeutic target for DR in the future. Full article

(This article belongs to the Special Issue Glycosylation in the Human Metabolism of Congenital Metabolic Diseases)

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