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Molecular Mechanisms and the Link Between Obesity, Diabetes and Inflammation
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Molecular Mechanisms and the Link Between Obesity, Diabetes and Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 January 2026 | Viewed by 883

Special Issue Editors

Dr. Maria Chiara Pelle

E-Mail Website
Guest Editor
Unit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, Italy
Interests: diabetes; obesity; metabolism
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Arturi Franco

E-Mail Website
Guest Editor
Unit of Internal Medicine, Department of Medical and Surgical Sciences, University “Magna Graecia” of Catanzaro, 88100 Catanzaro, Italy
Interests: diabetes; obesity; metabolism

Special Issue Information

Dear Colleagues,

Obesity and type 2 diabetes mellitus are considered a growing global health problem. They are now known to be major risk factors for chronic diseases, such as cardiovascular and metabolic diseases, which have become the main causes of morbidity and mortality in recent years. Obesity and diabetes are closely linked by a state of chronic low-grade inflammation that alters the insulin signaling pathway and leads to insulin resistance. Moreover, in recent years, there is evidence that a central role is played by the presence of dysfunctional adipose tissue, and several pathways that link the impairment of insulin resistance through obesity-induced inflammation have been identified, such as the activation of nuclear factor kappa B (NF-κB), cJun-N-terminal kinase (JNK), suppressor of cytokine signaling (SOCS) proteins, wingless-related integration site (Wnt), and Toll-like receptor (TLR) signaling pathways. This Special Issue focuses on investigating the link between metabolic alterations and chronic diseases and understanding how they perturb tissue function, leading to the detection of new molecules that can be used as biomarkers for the development of novel therapeutic targets.

Dr. Maria Chiara Pelle
Prof. Dr. Arturi Franco
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • adipose tissue
  • biomarkers
  • diabetes
  • inflammation
  • obesity
  • cytokine
  • insulin resistance
  • signaling pathways
  • metabolic diseases

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Published Papers (2 papers)

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Research

26 pages, 19416 KiB  
Article
Identification and Characterization of a Translational Mouse Model for Blood–Brain Barrier Leakage in Cerebral Small Vessel Disease
by Ruxue Jia, Gemma Solé-Guardia, Vivienne Verweij, Jessica M. Snabel, Bram Geenen, Anil Man Tuladhar, Robert Kleemann, Amanda J. Kiliaan and Maximilian Wiesmann
Int. J. Mol. Sci. 2025, 26(14), 6706; https://doi.org/10.3390/ijms26146706 - 12 Jul 2025
Viewed by 286
Abstract
Blood–brain barrier (BBB) dysfunction is a hallmark of cerebral small vessel disease (cSVD). This study aimed to identify a mouse model that replicates BBB impairment and shares key cSVD risk factors. Transgenic db/db and LDLr−/−.Leiden mice, both prone to obesity and [...] Read more.
Blood–brain barrier (BBB) dysfunction is a hallmark of cerebral small vessel disease (cSVD). This study aimed to identify a mouse model that replicates BBB impairment and shares key cSVD risk factors. Transgenic db/db and LDLr−/−.Leiden mice, both prone to obesity and hypertension, were compared to C57BL/6J controls. BBB leakage was assessed using DCE-MRI and sodium fluorescein (NaFl); cerebral blood flow (CBF) by MRI. Dyslipidemia and vascular inflammation were measured by plasma tests. Tight junction integrity, endothelial dysfunction (glucose transporter 1, GLUT-1) and neuroinflammation were evaluated with immunohistochemistry and PCR. Both transgenic models developed an obese phenotype with hyperinsulinemia, but only LDLr−/−.Leiden mice showed human-like dyslipidemia. When fed a high-fat diet (HFD) or HFD plus cholesterol, LDLr−/−.Leiden mice showed reduced CBF, endothelial dysfunction (lowered GLUT-1), elevated vascular inflammation (ICAM-1, VCAM-1, S-selectin), and BBB leakage, as evidenced by DCE-MRI and NaFl, together with reduced ZO-1 and claudin-5 expression. Contrastingly, db/db mice showed endothelial dysfunction without BBB leakage. Neuroinflammation (IBA-1, GFAP) was observed only in LDLr−/−.Leiden groups, consistent with BBB disruption. These findings indicate that LDLr−/−.Leiden mice, but not db/db mice, are a promising translational model for studying BBB dysfunction in cSVD, offering insights into disease mechanisms and a platform for therapeutic development. Full article
(This article belongs to the Special Issue Molecular Mechanisms and the Link Between Obesity, Diabetes and Inflammation)
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17 pages, 2477 KiB  
Article
The Purinergic Receptor P2X5 Modulates Glucose Metabolism and Expression of Thermogenic Genes in Brown Adipose Tissue
by Michelle Y. Jaeckstein, Lisa Miegel, Janina Behrens, Tobias Stähler, Björn-Philipp Diercks, Markus Heine, Friedrich Koch-Nolte and Joerg Heeren
Int. J. Mol. Sci. 2025, 26(13), 6474; https://doi.org/10.3390/ijms26136474 - 4 Jul 2025
Viewed by 348
Abstract
Next to adrenergic signalling, purinergic pathways mediated by extracellular adenine nucleotides have been described to shape thermogenic and metabolic functions in brown adipose tissue (BAT). Here we describe high expression of P2X5 that is activated by ATP in mature adipocytes of BAT and [...] Read more.
Next to adrenergic signalling, purinergic pathways mediated by extracellular adenine nucleotides have been described to shape thermogenic and metabolic functions in brown adipose tissue (BAT). Here we describe high expression of P2X5 that is activated by ATP in mature adipocytes of BAT and differentiated brown adipocytes in vitro. The levels of other P2X family members were much lower, or expression was restricted to tissue-resident macrophages or endothelial cells. Global and brown adipocyte-specific P2rx5 deficiency resulted in lower expression of the uncoupling protein 1 (UCP1). However, indirect calorimetry studies showed that P2X5 did not affect systemic energy expenditure. Of note, glucose tolerance was impaired under chow and obesogenic high-fat diet conditions, which can be explained by lower glucose disposal into BAT but not into other organs. In summary, these data indicate a modulatory role of P2X5 in systemic and BAT-specific glucose metabolism. Full article
(This article belongs to the Special Issue Molecular Mechanisms and the Link Between Obesity, Diabetes and Inflammation)
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