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Diabetes and Metabolic Dysfunction

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 October 2025 | Viewed by 999

Special Issue Editor


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Guest Editor
Department of Internal Medicine, Faculty of Medicine, University of Ioannina, 45110 Ioannina, Greece
Interests: internal medicine; dyslipidemia; metabolic syndrome; pharmacology

Special Issue Information

Dear Colleagues,

Type 2 diabetes mellitus is a complex metabolic disorder that affects nearly every organ in the human body. In addition to impaired glucose metabolism, the hallmark of the disease, numerous other metabolic abnormalities have been identified in patients with diabetes. Some of these abnormalities appear before a clinical diagnosis, while others emerge as the disease progresses, signaling its severity. Certain biomolecular markers indicate advanced disease and impending vascular complications. Identifying and understanding the molecular pathways and mechanisms underlying these metabolic disturbances can enhance our knowledge of type 2 diabetes pathophysiology and pathogenesis, facilitate earlier diagnoses, and predict complications. Moreover, targeting these abnormalities may offer new therapeutic avenues, potentially improving both the lifespan and quality of life of individuals with diabetes.

This Special Issue focuses on the molecular advances in diabetes and its complications. Original research and reviews on characteristic metabolic disorders, molecular therapies of diabetes, and its complications are welcome.

Since IJMS is a journal of molecular science, pure clinical or model studies will therefore not be suitable for our journal; however, clinical or pure model submissions with biomolecular experiments are welcomed.

Dr. Vasilis Tsimihodimos
Guest Editor

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Keywords

  • diabetes
  • metabolic dysfunction
  • glucose metabolism
  • metabolic disturbances
  • complications

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Published Papers (2 papers)

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Research

14 pages, 2264 KiB  
Article
The Beneficial Impact of a Novel Pancreatic Polypeptide Analogue on Islet Cell Lineage
by Wuyun Zhu, Neil Tanday, Peter R. Flatt and Nigel Irwin
Int. J. Mol. Sci. 2025, 26(9), 4215; https://doi.org/10.3390/ijms26094215 - 29 Apr 2025
Viewed by 124
Abstract
(Proline3)PP, or (P3)PP, is an enzymatically stable, neuropeptide Y4 receptor (NPY4R)-selective, pancreatic polypeptide (PP) analogue with established weight-lowering and pancreatic islet morphology benefits in obesity-diabetes. In the current study, we now investigate the impact of twice-daily (P3)PP administration (25 [...] Read more.
(Proline3)PP, or (P3)PP, is an enzymatically stable, neuropeptide Y4 receptor (NPY4R)-selective, pancreatic polypeptide (PP) analogue with established weight-lowering and pancreatic islet morphology benefits in obesity-diabetes. In the current study, we now investigate the impact of twice-daily (P3)PP administration (25 nmol/kg) for 11 days on islet cell lineage, using streptozotocin (STZ) diabetic Ins1Cre/+;Rosa26-eYFP and GluCreERT2;Rosa26-eYFP transgenic mice with enhanced yellow fluorescent protein (eYFP) labelling of beta-cell and alpha-cells, respectively. (P3)PP had no obvious impact on body weight or blood glucose levels in STZ-diabetic mice at the dose tested, but did return food intake towards control levels in Ins1Cre/+;Rosa26-eYFP mice. Notably, pancreatic insulin content was augmented by (P3)PP treatment in both Ins1Cre/+;Rosa26-eYFP and GluCreERT2;Rosa26-eYFP mice, alongside enhanced beta-cell area and reduced alpha-cell area. Beneficial (P3)PP-induced changes on islet morphology were consistently associated with decreased beta-cell apoptosis, while (P3)PP also augmented beta-cell proliferation in Ins1Cre/+;Rosa26-eYFP mice. Alpha-cell turnover rates were returned towards healthy control levels by (P3)PP intervention in both mouse models. In terms of islet cell lineage, increased transition of alpha- to beta-cells as well as decreased beta- to alpha-cell differentiation were shown to contribute towards the enhancement of beta-cell area in (P3)PP-treated mice. Together these data reveal, for the first time, sustained NPY4R activation positively modulates beta-cell turnover, as well as islet cell plasticity, to help preserve pancreatic islet architecture following STZ-induced metabolic stress. Full article
(This article belongs to the Special Issue Diabetes and Metabolic Dysfunction)
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16 pages, 1067 KiB  
Article
A Retrospective Analysis of the Changes in Prediabetes-Associated Markers of Thyroid Function in Patients from Durban, South Africa
by Hasnaa Satar Aswani, Wendy Mdluli and Andile Khathi
Int. J. Mol. Sci. 2025, 26(5), 2170; https://doi.org/10.3390/ijms26052170 - 28 Feb 2025
Viewed by 450
Abstract
Thyroid dysfunction and type 2 diabetes melittus (T2DM) are two of the most common endocrine disorders, and the emerging condition of prediabetes necessitates additional research to better understand the complex interactions between thyroid hormones, metabolic regulation, and the progression from prediabetes to T2DM. [...] Read more.
Thyroid dysfunction and type 2 diabetes melittus (T2DM) are two of the most common endocrine disorders, and the emerging condition of prediabetes necessitates additional research to better understand the complex interactions between thyroid hormones, metabolic regulation, and the progression from prediabetes to T2DM. This study sought to investigate changes in selected markers of thyroid function in patients with pre-diabetes. Upon obtaining ethics permission, blood samples were collected from patients in King Edward Hospital in Durban, South Africa. The samples were classified as non-diabetic, pre-diabetic, and type 2 diabetic using the ADA guidelines. The thyroid stimulating hormone (TSH), thyroxine (T4) triiodothyronine (T3), Thyroglobulin (TG), and thyroid peroxidase antibody (TPOAb) concentrations were determined in these samples. The results showed elevated TSH, decreased T3 and T4, decreased thyroglobulin (Tg), and elevated TPOAb in the prediabetic group which became considerably pronounced with the shift to T2DM. The alterations in these markers during prediabetes may indicate an early stage of thyroid dysfunction necessitating further investigation as these alterations become more pronounced during type 2 diabetes mellitus. Full article
(This article belongs to the Special Issue Diabetes and Metabolic Dysfunction)
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