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Internal Medicine, Clinical Immunology and Metabolic Diseases

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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 (20 December 2023) | Viewed by 4855

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Special Issue Editors

Dr. Geoffrey Urbanski

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Guest Editor

Department of Orofacial Sciences, CoLabs, Medical Sciences Building, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA
Interests: sjogren's syndrome; antiphospholipid syndrome; immune diseases; cobalamin-dependent pathways; omics

Dr. Floris Chabrun

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Guest Editor

Laboratory of Biochemistry and Molecular Biology, University Hospital of Angers, 4 rue Larrey, CEDEX 9, 49933 Angers, Pays de la Loire, France
Interests: omics; artificial intelligence; machine learning; deep learning

Special Issue Information

Dear Colleagues,

For a long time, immunity and metabolism have been considered as separate fields of research with little connections/gateways. However, over the last decade, hypothesis-free approaches have demonstrated the involvement of immune cells in metabolic diseases, but also the imbalance of metabolic pathways in immune diseases.

On one hand, it is now obvious that the immune system is not limited to conferring anti-infectious and anti-neoplastic protection but is also pivotal in metabolism homeostasis. Perturbations in this intricate immune–metabolism crosstalk contribute to disorders such as metabolic syndrome and solid cancers.

On the other hand, metabolism plays a crucial role in the maintenance of correct immune responses through the regulation of intracellular signal transduction and intercellular communication far beyond the reactive oxygen species. The SARS-CoV-2 pandemic has shed light on the dramatic consequences of ‘metabolic’ morbidities such as diabetes and obesity on the immune cells and the infection course. Studying the metabolism of immune cells would provide new insights into some still-unraveled functions of immune cells.

This Special Issue of Metabolites, “Internal Medicine, Clinical Immunology and Metabolic Diseases”, will be dedicated to dealing with interactions between immunity and metabolism in both immune and metabolic diseases. This Special Issue is intended for basic research, but also translational and clinical studies, as well as both hypothesis-led and hypothesis-free studies.

Dr. Geoffrey Urbanski
Dr. Floris Chabrun
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

autoimmune diseases
metabolic disorders
immunity
omics
hypothesis-free research
machine learning

Published Papers (3 papers)

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Research

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12 pages, 4154 KiB

Open AccessArticle

Anti-Hyperuricemic Effects of Extracts from Chaenomeles speciosa (Sweet) Nakai Fruits on Hyperuricemic Rats

by Ruoling Xu, Peng Deng, Yiren Ma, Kui Li, Fucai Ren and Ning Li

Metabolites 2024, 14(2), 117; https://doi.org/10.3390/metabo14020117 - 10 Feb 2024

Viewed by 1150

Abstract

Chaenomeles speciosa (Sweet) Nakai (C. speciosa) fruit has medicinal and food applications and exhibits beneficial pharmacological properties. This study aimed to explore the hypouricemic effect of C. speciosa fruit extracts on hyperuricemic rats and uncover potential protective mechanisms. The rats were given hypoxanthine (HX, 100 mg/kg) and potassium oxonate (PO, 300 mg/kg) for 14 days to induce hyperuricemia. Subsequently, the rats were orally administered C. speciosa fruits total extract (CSFTE, 250, 500, and 1000 mg/kg) and allopurinol (AP, 10 mg/kg) one hour after exposure to HX and PO. The results showed that CSFTE had significant xanthine oxidase (XOD) inhibitory activity in vitro (IC₅₀ value of 334.2 μg/mL) and exhibited hypouricemic effects in vivo, reducing uric acid (UA), creatinine (CRE), and blood urea nitrogen (BUN) levels in serum. CSFTE increased UA excretion through the regulation of URAT1, GLUT9, OAT1, and OAT3 protein expression in the kidneys of hyperuricemic rats. Additionally, CSFTE (500 and 1000 mg/kg) was more effective than AP in improving renal injury and protecting kidney function in hyperuricemic rats. Our study demonstrated that CSFTE effectively reduced UA levels and protected the kidneys by inhibiting XOD expression in vitro and regulating UA, CRE, BUN, URAT1, GLUT9, OAT1, and OAT3 proteins in vivo. Full article

(This article belongs to the Special Issue Internal Medicine, Clinical Immunology and Metabolic Diseases)

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17 pages, 3790 KiB

Open AccessArticle

Biomarkers of Metabolic Adaptation to High Dietary Fats in a Mouse Model of Obesity Resistance

by Fadia Milhem, Leah M. Hamilton, Emily Skates, Mickey Wilson, Suzanne D. Johanningsmeier and Slavko Komarnytsky

Metabolites 2024, 14(1), 69; https://doi.org/10.3390/metabo14010069 - 20 Jan 2024

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Abstract

Obesity-resistant (non-responder, NR) phenotypes that exhibit reduced susceptibility to developing obesity despite being exposed to high dietary fat are crucial in exploring the metabolic responses that protect against obesity. Although several efforts have been made to study them in mice and humans, the individual protective mechanisms are poorly understood. In this exploratory study, we used a polygenic C57BL/6J mouse model of diet-induced obesity to show that NR mice developed healthier fat/lean body mass ratios (0.43 ± 0.05) versus the obesity-prone (super-responder, SR) phenotypes (0.69 ± 0.07, p < 0.0001) by upregulating gene expression networks that promote the accumulation of type 2a, fast-twitch, oxidative muscle tissues. This was achieved in part by a metabolic adaptation in the form of blood glucose sparing, thus aggravating glucose tolerance. Resistance to obesity in NR mice was associated with 4.9-fold upregulated mitoferrin 1 (Slc25a37), an essential mitochondrial iron importer. SR mice also showed fecal volatile metabolite signatures of enhanced short-chain fatty acid metabolism, including increases in detrimental methyl formate and ethyl propionate, and these effects were reversed in NR mice. Continued research into obesity-resistant phenotypes can offer valuable insights into the underlying mechanisms of obesity and metabolic health, potentially leading to more personalized and effective approaches for managing weight and related health issues. Full article

(This article belongs to the Special Issue Internal Medicine, Clinical Immunology and Metabolic Diseases)

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Review

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16 pages, 1435 KiB

Open AccessReview

Progression to Obesity: Variations in Patterns of Metabolic Fluxes, Fat Accumulation, and Gastrointestinal Responses

by Fadia Milhem and Slavko Komarnytsky

Metabolites 2023, 13(9), 1016; https://doi.org/10.3390/metabo13091016 - 15 Sep 2023

Cited by 3 | Viewed by 1645

Abstract

Obesity is a multifactorial disorder that is remarkably heterogeneous. It presents itself in a variety of phenotypes that can be metabolically unhealthy or healthy, associate with no or multiple metabolic risk factors, gain extreme body weight (super-responders), as well as resist obesity despite the obesogenic environment (non-responders). Progression to obesity is ultimately linked to the overall net energy balance and activity of different metabolic fluxes. This is particularly evident from variations in fatty acids oxidation, metabolic fluxes through the pyruvate-phosphoenolpyruvate-oxaloacetate node, and extracellular accumulation of Krebs cycle metabolites, such as citrate. Patterns of fat accumulation with a focus on visceral and ectopic adipose tissue, microbiome composition, and the immune status of the gastrointestinal tract have emerged as the most promising targets that allow personalization of obesity and warrant further investigations into the critical issue of a wider and long-term weight control. Advances in understanding the biochemistry mechanisms underlying the heterogenous obesity phenotypes are critical to the development of targeted strategies to maintain healthy weight. Full article

(This article belongs to the Special Issue Internal Medicine, Clinical Immunology and Metabolic Diseases)

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