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Metabolites
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Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 2nd...
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Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 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: 30 June 2026 | Viewed by 4111

Special Issue Editors

Prof. Dr. Tiemin Liu

E-Mail Website
Guest Editor
Department of Physiology and Biophysics, the School of Life Science, Fudan University, Shanghai 200438, China
Interests: physiology and neuroscience; neuromodulation; pathogenesis of metabolic disorders and neuroendocrine homeostasis in mammals; muscle and exercise
Special Issues, Collections and Topics in MDPI journals
Dr. Hongmei Yan

E-Mail Website
Guest Editor
Department of Endocrinology, Zhongshan Hospital, Fudan University, Shanghai 200032, China
Interests: obesity; non-alcoholic fatty liver disease; metabolic syndrome; sarcopenia
Special Issues, Collections and Topics in MDPI journals
Dr. Qiongyue Zhang

E-Mail Website
Guest Editor
Department of Endocrinology, Huashan Hospital, Fudan University, Shanghai 200032, China
Interests: obesity; type 2 diabetes; standardized and individualized diagnosis and treatment of metabolic diseases; bariatric surgery, especially the preoperative evaluation and postoperative follow-up of differential diagnosis of obesity and perioperative blood glucose management
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the face of escalating global health challenges, the intricate web linking obesity, diabetes, and metabolic syndrome has emerged as a forefront concern for researchers, clinicians, and public health policymakers. This Special Issue of Metabolites aims to delve into the complexities of these interrelated conditions, with a specific focus on unraveling their pathogenesis. By casting a spotlight on the root causes and mechanisms underlying these diseases, we aspire to foster a deeper understanding that could eventually pave the way for innovative prevention and treatment strategies.

The epidemic proportions of obesity and its consequent cascade effect—propelling the rise in type 2 diabetes and metabolic syndrome instances worldwide—necessitate a multifaceted examination. This pursuit is not merely academic; it has the potential to significantly alter the course of countless lives through informed intervention strategies and therapeutic advancements.

We invite contributors to explore a broad spectrum of topics within this theme, including, but not limited to, the following:

  1. Genetic predispositions and molecular biological insights into obesity, diabetes, and metabolic syndrome.
  2. The impact of lifestyle factors (diet, physical activity, sleep, and stress) on the manifestation and progression of these diseases.
  3. The role of the microbiome and environmental exposures in disease pathogenesis.
  4. The potential of multi-omics in uncovering novel pathways and targets, such as metabolomics, lipidomics, proteomics, genomics, etc.
  5. The role of inflammation and oxidative stress in these metabolic diseases.
  6. Pathophysiological mechanisms about how obesity, diabetes, and metabolic syndrome interact and potentiate each other.

This Special Issue aims to be a crucible of innovation, gathering under its aegis the latest research findings, insightful reviews, and forward-thinking perspectives. Our goal is to inspire a cross-disciplinary dialogue that spans the spectrum from molecular biology to societal interventions, weaving together a comprehensive narrative on the pathogenesis of obesity, diabetes, and metabolic syndrome.

We welcome submissions in the form of original research articles, clinical trials, reviews, and perspectives that contribute meaningfully to our understanding of these conditions and offer glimpses into future directions for research and application. Contributions should aim not only to map the current landscape but also to identify gaps in our knowledge and propose pathways towards solutions.

Together, through this Special Issue, let us create a collaborative platform for sharing cutting-edge research and innovative ideas, igniting conversations that could lead to groundbreaking transformations in how these pervasive health issues are understood and addressed. Submissions are now open; we look forward to receiving contributions that enrich this critical discourse.

Prof. Dr. Tiemin Liu
Dr. Hongmei Yan
Dr. Qiongyue Zhang
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 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

  • metabolic diseases: obesity, diabetes, NAFLD, MAFLD, NASH, metabolic syndrome, etc.
  • multi-omics: metabolomics, lipidomics, proteomics, etc.
  • pathogenesis: genetic predispositions, lifestyle factors, microbiome and environmental exposures, etc.

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Related Special Issue

Published Papers (4 papers)

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Research

11 pages, 315 KB  
Article
Validation of a Diabetes Subtype Classification Model Using Data from U.S. Adults Before and After the COVID-19 Pandemic
by Brian Lu, Peng Li, Andrew B. Crouse, Tiffany Grimes, Ava N. Smith, Matthew Might, Fernando Ovalle and Anath Shalev
Metabolites 2026, 16(3), 204; https://doi.org/10.3390/metabo16030204 - 19 Mar 2026
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Abstract
Background: We (and others) have previously identified five clinically distinct diabetes subtypes. Currently, few models to identify diabetes subtypes are readily accessible. Further, while COVID-19 has been associated with increased risk of new-onset diabetes, it remains unknown whether the pandemic is also associated [...] Read more.
Background: We (and others) have previously identified five clinically distinct diabetes subtypes. Currently, few models to identify diabetes subtypes are readily accessible. Further, while COVID-19 has been associated with increased risk of new-onset diabetes, it remains unknown whether the pandemic is also associated with changes in diabetes subtype distribution. Methods: We used the electronic health records of patients diagnosed with diabetes from 2010 to 2019 at the Kirklin Clinic of the University of Alabama at Birmingham (UAB) to train models to assign diabetes subtypes previously identified by hierarchical clustering. We then applied the trained model to conduct a retrospective cluster analysis of electronic health records of patients diagnosed with diabetes from 2020 to 2024 at UAB. We further validated our findings using data from the 2015–2023 National Health and Nutrition Examination Surveys (NHANES). Results: The trained classification model had an average specificity of 98% and an average sensitivity of 93%. Using the model, we identified a significant difference in the distribution of type 2 diabetes subtypes in patients at UAB and in participants in NHANES. In particular, the proportion of patients with severe insulin-dependent diabetes or severe insulin-resistant diabetes subtypes increased from 42% to 61% and 31% to 40% at the UAB and in NHANES, respectively. Conclusions: The model presented here can facilitate the identification of diabetes subtypes. The proportions of patients with severe subtypes of diabetes have seemed to increase in the more recent years following the pandemic. Further studies are required to determine the potential causes of this phenomenon. Full article
(This article belongs to the Special Issue Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 2nd Edition)
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21 pages, 1738 KB  
Article
Tissue-Specific Multi-Omics Integration Demonstrates Molecular Signatures Connecting Obesity to Immune Vulnerability
by Ozge Onluturk Aydogan, Aytac Dursun Oksuzoglu and Beste Turanli
Metabolites 2026, 16(2), 95; https://doi.org/10.3390/metabo16020095 - 27 Jan 2026
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Abstract
Background: Adipose tissue surrounds organs and tissues in the body and can alter their function. It could secrete diverse biological molecules, including lipids, cytokines, hormones, and metabolites. In light of all this information, obesity can influence many tissues and organs in the body, [...] Read more.
Background: Adipose tissue surrounds organs and tissues in the body and can alter their function. It could secrete diverse biological molecules, including lipids, cytokines, hormones, and metabolites. In light of all this information, obesity can influence many tissues and organs in the body, and this situation makes obesity a central contributor to multiple disorders. It is very important to investigate the crosstalk between tissues and organs in the body to clarify the key mechanisms of obesity. Methods: In this study, we analyzed the gene expression profiles of the liver, skeletal muscle, blood, visceral, and subcutaneous adipose tissue. Differentially expressed genes (DEGs) were identified for each tissue, and functional enrichment and protein–protein interaction network analyses were performed on genes commonly identified across tissues. Priority candidate genes were identified using network-based centrality measures, and potential molecular intersection points were explored through host-pathogen interaction network analysis. This study provides an integrative framework for characterizing inter-tissue molecular patterns associated with obesity at the network level. Results: The muscle, subcutaneous adipose tissue, and blood have the highest number of DEGs. The subcutaneous adipose tissue and blood stand out due to the number of DEGs they possess, although liver and visceral adipose tissue have lower amounts. Cancer ranks first in terms of diseases associated with obesity, and this association is accompanied by leukemia, lymphoma, and gastric cancer. RPL15 and RBM39 are the top genes in both degree and betweenness metrics. The host–pathogen interaction network consists of 13 unique-host proteins, 54 unique-pathogen proteins, and 27 unique-pathogen organisms, and the Influenza A virus had the highest interaction. There were a small number of common metabolites in all tissues: 2-Oxoglutarate, Adenosine, Succinate, and D-mannose. Conclusions: In this study, we aimed to identify candidate molecules for obesity using an integrative approach, examining the gene profiles of different organs and tissues. The findings of this study suggest a possible link between obesity and immune-related biological processes. The network obtained from the host-pathogen interaction analysis, and especially the pathways associated with viral infections that stand out in the functional enrichment analysis, may overlap with molecular signatures linked to obesity. Furthermore, the co-occurrence of cytokine signaling, insulin, and glucose metabolism pathways in the enrichment results indicates that the response of cells to insulin may be affected in obese individuals, suggesting a potential interaction between immune and metabolic processes; however, further experimental validation is needed to reveal the direct functional effects of these relationships. Full article
(This article belongs to the Special Issue Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 2nd Edition)
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13 pages, 7859 KB  
Article
Itaconate Promotes Cold Adaptation and Myocardial Protection by Enhancing Brown Adipose Tissue Metabolism
by Zilong Geng, Xing Liu, Xiao Cheng, Shizhan Xu, Jin Zhang, Ao Tan, Shun Song and Shasha Zhang
Metabolites 2026, 16(1), 66; https://doi.org/10.3390/metabo16010066 - 12 Jan 2026
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Abstract
Background/Objectives: Itaconic acid (ITA) is an immunometabolite with anti-inflammatory and metabolic regulatory functions, but its cellular source and role in brown adipose tissue (BAT) remain unclear. This study aims to reveal the expression patterns of the key ITA synthesis gene Irg1 in BAT [...] Read more.
Background/Objectives: Itaconic acid (ITA) is an immunometabolite with anti-inflammatory and metabolic regulatory functions, but its cellular source and role in brown adipose tissue (BAT) remain unclear. This study aims to reveal the expression patterns of the key ITA synthesis gene Irg1 in BAT at different developmental stages and to investigate the effects of cold exposure and exogenous ITA on BAT metabolic function and cardioprotection. Methods: Single-cell RNA sequencing was used to analyze the gene expression profiles of stromal vascular fraction (SVF) cells in BAT from P7 neonatal and adult mice. Bioinformatic methods were applied to identify cell types expressing Irg1. Cold exposure (4 °C) and exogenous ITA treatment were employed to evaluate BAT morphology, and the ITA content in BAT was detected using gas chromatography–triple quadrupole mass spectrometry, UCP1 protein expression, and body temperature changes. A transverse aortic constriction (TAC) surgery model was established to induce cardiac dysfunction, and BAT excision was performed to explore the BAT-dependent effects of ITA on myocardial hypertrophy, fibrosis, and cardiac function. Results: In P7 neonatal mouse BAT, Irg1 was predominantly expressed in a subset of interferon-responsive activated macrophages (macrophage27), while in adult mice, it was mainly expressed in neutrophils and a functionally similar macrophage subset (macrophage25). Cold exposure significantly suppressed Irg1 expression in neutrophils but did not affect its expression in macrophages, also resulting in a significant decrease in ITA content in BAT. Exogenous ITA significantly enhanced BAT thermogenesis under cold conditions, which manifested as reduced lipid droplets, upregulated UCP1 expression, and increased body temperature. In the TAC model, ITA treatment markedly improved cardiac function, attenuated myocardial hypertrophy and fibrosis, and these protective effects were significantly diminished after BAT excision. Conclusions: ITA promotes cold adaptation and ameliorates cardiac injury by enhancing BAT metabolic function, and its effects depend on the presence of BAT. This study provides new insights for the treatment of metabolic cardiovascular diseases. Full article
(This article belongs to the Special Issue Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 2nd Edition)
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12 pages, 1792 KB  
Article
Chronic Intermittent Low-Pressure Hypoxia Suppresses Inflammation and Regulates Glycolipids by Modulating Mitochondrial Respiration in db/db Mice
by Xin Jiang, Keqing Yuan, Xiaofeng Ge, Lili Yu, Yufei Cui, Lianhai Jin and Ying Chang
Metabolites 2025, 15(11), 707; https://doi.org/10.3390/metabo15110707 - 30 Oct 2025
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Abstract
Background/Objectives: Type 2 Diabetes Mellitus (T2DM) is a chronic disease with persistent hyperglycemia as the main clinical manifestation. Chronic Intermittent Hypobaric Hypoxia (CIHH) is a clinical intervention with intermittent low-pressure hypoxic environmental stimulation. The aim of this study was to evaluate the [...] Read more.
Background/Objectives: Type 2 Diabetes Mellitus (T2DM) is a chronic disease with persistent hyperglycemia as the main clinical manifestation. Chronic Intermittent Hypobaric Hypoxia (CIHH) is a clinical intervention with intermittent low-pressure hypoxic environmental stimulation. The aim of this study was to evaluate the therapeutic effect and anti-inflammatory effect of CIHH in db/db mice. Methods: A simulated 5000 m altitude environment was used to intervene db/db mice. db/db mice were divided into an intervention group (6 h/d) (n = 10) and a control group (n = 10); meanwhile, healthy mice were divided into two groups, the intervention group (6 h/d) (n = 10) and the control group (n = 10). The intervention lasted for 6 weeks. Biochemical analyses and pathological tests were performed to evaluate the therapeutic effects, and for the evaluation of mitochondrial respiration, changes in the respiratory capacity of liver mitochondria at various stages of respiration were examined using Oxygraph-2 k. Changes in inflammatory factors in the liver of mice were analyzed using ELISA. Results: Following CIHH intervention, db/db mice exhibited significant reductions in body weight, food intake, FBG, TC, TG, and LDL, along with increased HDL levels. Liver indices, PEPCK, G-6-phosphate dehydrogenase, and GLUT2 decreased, while GLUT4 and p-AMPK increased. Hepatic HE staining revealed reduced lipid droplets in the liver. HOMA-IR decreased while HOMA-IS increased. Hepatocyte mitochondrial respiration-related indicators CI + CII stage RCR, CII stage RCR, and CI stage SCR increased, while CI stage SCR decreased. Inflammation-related factors NLRP3, TNF-α, IL-1β, and IL-6 decreased in liver tissue. Conclusions: CIHH effectively improves gluconeogenesis and insulin resistance in db/db mice, a result potentially linked to enhanced mitochondrial respiratory capacity and anti-inflammatory effects. Therefore, CIHH offers a potential therapeutic approach for type 2 diabetes. Full article
(This article belongs to the Special Issue Exploring Pathological Mechanisms in Obesity, Diabetes, and Metabolic Syndrome: 2nd Edition)
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