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Diabetes and Its Complications: From Molecular Mechanisms to Novel Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 3562

Special Issue Editor

Dr. Andrea Paola Rojas Gil

E-Mail Website
Guest Editor
Department of Nursing, Faculty of Health Sciences, University of Peloponnese, 22100 Tripoli, Greece
Interests: diabetes; nutrition; oncology; metabolisms
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia due insulin insufficiency or impaired insulin action. Diabetes could affects the quality of life and survival of patients. Recent data from the International Diabetes Federation showed that by 2045 it is expected to reach 783 million patients. Diabetes carries an increased risk for cardiovascular diseases including kidney failure. Different elements of the environment have been posited to influence the appearance of diabetes mellitus. Sleep and diet are key factors in regulating glucose metabolism, which is also significantly affected by physical activity. Air pollution has been shown to change endothelial function, and systemic inflammation, and trigger insulin resistance. The genetic background determines the predisposition to develop diabetes while the autoimmune related to diabetes seems to be also determined by environmental triggers, such as endocrine disrupting chemicals (EDCs). This Special Issue of the International Journal of Molecular Sciences focuses on the molecular and metabolic mechanism related to the appearance and complications of diabetes, emphasizing on environmental factors, and possible applications related to interventions and therapy.

Dr. Andrea Paola Rojas Gil
Guest Editor

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. 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

  • diabetes
  • diabetes complications
  • enviromental factors
  • endocrine disruptors
  • nutrition
  • sleep
  • therapy
  • molecular mechanisms

Published Papers (3 papers)

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Research

20 pages, 20927 KiB  
Article
Serotonin and Interleukin 10 Can Influence the Blood and Urine Viscosity in Gestational Diabetes Mellitus and Pregnancy-Specific Urinary Incontinence
by Danielle Cristina Honório França, Adenilda Cristina Honorio-França, Kênia Maria Rezende Silva, Fernanda Cristina Bérgamo Alves, Gabriela Bueno, Sarah Maria Barneze Costa, Aron Carlos de Melo Cotrim, Angélica Mércia Pascon Barbosa, Eduardo Luzía França, Marilza Vieira Cunha Rudge and The Diamater Study Group
Int. J. Mol. Sci. 2023, 24(24), 17125; https://doi.org/10.3390/ijms242417125 - 05 Dec 2023
Viewed by 850
Abstract
Serotonin and interleukin 10 (IL-10) may play a role in gestational diabetes mellitus. Hyperglycemic environment, the detrusor musculature of the bladder and pelvic floor muscles may become damaged, leading to urination problems and urine viscosity in pregnant women with gestational diabetes mellitus and [...] Read more.
Serotonin and interleukin 10 (IL-10) may play a role in gestational diabetes mellitus. Hyperglycemic environment, the detrusor musculature of the bladder and pelvic floor muscles may become damaged, leading to urination problems and urine viscosity in pregnant women with gestational diabetes mellitus and pregnancy-specific urinary incontinence. Urine and blood samples were collected from pregnant women between 24 and 28 weeks of gestation. The serotonin concentration and cytokine IL-10 levels were evaluated in plasma and urine. In the total blood and urine, the viscosity was evaluated in the presence and absence of exogenous serotonin and IL-10. The plasma serotonin levels decreased, while the urine serotonin levels increased in the normoglycemic incontinent (NG-I), hyperglycemic continent (GDM-C), and hyperglycemic incontinent (GDM-I) groups. The IL-10 in the plasma decreased in the GDM-I group and was higher in the urine in the NG-I and GDM-I groups. The blood viscosity was higher, independently of urinary incontinence, in the GDM groups. The serotonin increased the blood viscosity from women with GDM-C and urine in the NG-I, GDM-C, and GDM-I groups. Blood and urine in the presence of IL-10 showed a similar viscosity in all groups studied. Also, no difference was observed in the viscosity in either the blood or urine when in the presence of serotonin and IL-10. These findings suggest that serotonin and IL-10 have the potential to reduce blood viscosity in pregnant women with gestational diabetes and specific urinary incontinence, maintaining values similar to those in normoglycemic women’s blood. Full article
(This article belongs to the Special Issue Diabetes and Its Complications: From Molecular Mechanisms to Novel Therapeutic Approaches)
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17 pages, 1965 KiB  
Article
The Response of Antioxidant Enzymes and Antiapoptotic Markers to an Oral Glucose Tolerance Test (OGTT) in Children and Adolescents with Excess Body Weight
by Maria Efthymia Katsa, Eirini Kostopoulou, Tzortzis Nomikos, Anastasios Ioannidis, Vasileios Sarris, Spyridon Papadogiannis, Bessie E. Spiliotis and Andrea Paola Rojas Gil
Int. J. Mol. Sci. 2023, 24(22), 16517; https://doi.org/10.3390/ijms242216517 - 20 Nov 2023
Viewed by 770
Abstract
Oxidative stress and apoptosis are involved in the pathogenesis of obesity-related diseases. This observational study investigates the antioxidant and apoptotic markers response to an oral glucose tolerance test (OGTT) in a population of overweight children and adolescents, with normal (NGT) or impaired glucose [...] Read more.
Oxidative stress and apoptosis are involved in the pathogenesis of obesity-related diseases. This observational study investigates the antioxidant and apoptotic markers response to an oral glucose tolerance test (OGTT) in a population of overweight children and adolescents, with normal (NGT) or impaired glucose tolerance (IGT). Glucose, insulin, and C-peptide concentrations, as well as oxidative stress (SOD, GPx3) and apoptotic markers (Apo1fas, cck18), were determined at T = 0, 30, 60, 90, 120, and 180 min after glucose intake during OGTT. The lipid profile, thyroid function, insulin-like growth factor1, leptin, ghrelin, and adiponectin were also measured at baseline. The 45 participants, with a mean age of 12.15 (±2.3) years old, were divided into two subcategories: those with NGΤ (n = 31) and those with IGT (n = 14). The area under the curve (AUC) of glucose, insulin, and C-peptide was greater in children with IGT; however, only glucose differences were statistically significant. SOD and GPx3 levels were higher at all time points in the IGT children. Apo1fas and cck18 levels were higher in the NGT children at most time points, whereas Adiponectin was lower in the IGT group. Glucose increased during an OGTT accompanied by a simultaneous increase in antioxidant factors, which may reflect a compensatory mechanism against the impending increase in oxidative stress in children with IGT. Full article
(This article belongs to the Special Issue Diabetes and Its Complications: From Molecular Mechanisms to Novel Therapeutic Approaches)
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10 pages, 1217 KiB  
Article
Regulatory Roles of Histone Deacetylation in Metabolic Stress-Induced Expression of Caspase Recruitment Domain-Containing Protein 9 (CARD9) in Pancreatic β-Cells
by Mirabela Hali, Nelson Pinto, Noah Gleason and Anjaneyulu Kowluru
Int. J. Mol. Sci. 2023, 24(21), 15994; https://doi.org/10.3390/ijms242115994 - 06 Nov 2023
Viewed by 1538
Abstract
CARD9, a scaffolding protein, has been implicated in the pathogenesis of metabolic diseases, including obesity and diabetes. We recently reported novel roles for CARD9 in islet β-cell dysregulation under duress of gluco (HG)- and glucolipotoxic (GLT) stress. CARD9 expression was also increased in [...] Read more.
CARD9, a scaffolding protein, has been implicated in the pathogenesis of metabolic diseases, including obesity and diabetes. We recently reported novel roles for CARD9 in islet β-cell dysregulation under duress of gluco (HG)- and glucolipotoxic (GLT) stress. CARD9 expression was also increased in β-cells following exposure to HG and GLT stress. The current study is aimed at understanding the putative roles of histone deacetylation in HG- and GLT-induced expression of CARD9. Using two structurally distinct inhibitors of histone deacetylases (HDACs), namely trichostatin (TSA) and suberoylanilide hydroxamic acid (SAHA), we provide the first evidence to suggest that the increased expression of CARD9 seen under duress of HG and GLT stress is under the regulatory control of histone deacetylation. Interestingly, the expression of protein kinase Cδ (PKCδ), a known upstream regulator of CARD9 activation, is also increased under conditions of metabolic stress. However, it is resistant to TSA and SAHA, suggesting that it is not regulated via histone deacetylation. Based on these data, we propose that targeting the appropriate HDACs, which mediate the expression (and function) of CARD9, might be the next step to further enhance our current understanding of the roles of CARD9 in islet dysfunction under metabolic stress and diabetes. Full article
(This article belongs to the Special Issue Diabetes and Its Complications: From Molecular Mechanisms to Novel Therapeutic Approaches)
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