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Current Research on Diabetes and Metabolic Syndrome
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Current Research on Diabetes and Metabolic Syndrome

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: closed (28 February 2024) | Viewed by 6879

Special Issue Editor

Prof. Dr. Natalija Filipović

E-Mail Website
Guest Editor
Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Šoltanska 2, 21000 Split, Croatia
Interests: microvascular and macrovascular complications of diabetes; diabetic nephropathy; renal physiology and pathology; gene expression during embryonic and foetal development; kidneys and urinary system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetes and metabolic syndrome are among the leading public health problems in modern society, with increasing incidence. According to some estimations, over a billion people globally are affected by metabolic syndrome, while the International Diabetes Federation projects that the number of adults with diabetes worldwide will increase to 693 million by 2045. Despite the increase in the number of studies focused on these issues, there are still many gaps in our knowledge about the pathogenesis of metabolic syndrome and diabetic complications. In addition, current therapeutic approaches are limited in terms of their effectiveness. A large number of patients do not respond to specific therapeutic approaches, and results are often limited. Moreover, new promising strategies to prevent DM complications appear to carry serious side effects (ketoacidosis, increased risk of amputation, and genitourinary system infections). Therefore, new prevention and therapeutic strategies are needed, based on the understanding brought about by new scientific research. Therefore, we invite researchers to submit original papers or review articles that contribute to our knowledge about the pathogenesis of diabetic complications and metabolic syndrome, and/or reveal potential new strategies for their prevention and treatment.

Prof. Dr. Natalija Filipović
Guest Editor

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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.

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Keywords

  • diabetes
  • metabolic syndrome
  • obesity
  • insulin resistance
  • diabetic neuropathy
  • diabetic kidney disease
  • diabetic retinopathy
  • coronary heart disease
  • cardiomyopathy
  • cerebrovascular disease
  • peripheral artery disease

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Published Papers (4 papers)

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Research

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27 pages, 7268 KiB  
Article
Adropin Is Expressed in Pancreatic Islet Cells and Reduces Glucagon Release in Diabetes Mellitus
by Ifrah I. Ali, Crystal D’Souza, Saeed Tariq and Ernest A. Adeghate
Int. J. Mol. Sci. 2024, 25(18), 9824; https://doi.org/10.3390/ijms25189824 - 11 Sep 2024
Viewed by 1091
Abstract
Diabetes mellitus affects 537 million adults around the world. Adropin is expressed in different cell types. Our aim was to investigate the cellular localization in the endocrine pancreas and its effect on modulating pancreatic endocrine hormone release in streptozotocin (STZ)-induced diabetic rats. Adropin [...] Read more.
Diabetes mellitus affects 537 million adults around the world. Adropin is expressed in different cell types. Our aim was to investigate the cellular localization in the endocrine pancreas and its effect on modulating pancreatic endocrine hormone release in streptozotocin (STZ)-induced diabetic rats. Adropin expression in the pancreas was investigated in normal and diabetic rats using immunohistochemistry and immunoelectron microscopy. Serum levels of insulin, glucagon pancreatic polypeptide (PP), and somatostatin were measured using a Luminex® χMAP (Magpix®) analyzer. Pancreatic endocrine hormone levels in INS-1 832/3 rat insulinoma cells, as well as pancreatic tissue fragments of normal and diabetic rats treated with different concentrations of adropin (10−6, 10−9, and 10−12 M), were measured using ELISA. Adropin was colocalized with cells producing either insulin, glucagon, or PP. Adropin treatment reduced the number of glucagon-secreting alpha cells and suppressed glucagon release from the pancreas. The serum levels of GLP-1 and amylin were significantly increased after treatment with adropin. Our study indicates a potential role of adropin in modulating glucagon secretion in animal models of diabetes mellitus. Full article
(This article belongs to the Special Issue Current Research on Diabetes and Metabolic Syndrome)
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18 pages, 2153 KiB  
Article
Association of Glutathione Peroxidase 3 (GPx3) and miR-196a with Carbohydrate Metabolism Disorders in the Elderly
by Adam Włodarski, Izabela Szymczak-Pajor, Jacek Kasznicki, Egle Morta Antanaviciute, Bożena Szymańska and Agnieszka Śliwińska
Int. J. Mol. Sci. 2024, 25(10), 5409; https://doi.org/10.3390/ijms25105409 - 15 May 2024
Cited by 1 | Viewed by 1537
Abstract
The escalating prevalence of carbohydrate metabolism disorders (CMDs) prompts the need for early diagnosis and effective markers for their prediction. Hyperglycemia, the primary indicator of CMDs including prediabetes and type 2 diabetes mellitus (T2DM), leads to overproduction of reactive oxygen species (ROS) and [...] Read more.
The escalating prevalence of carbohydrate metabolism disorders (CMDs) prompts the need for early diagnosis and effective markers for their prediction. Hyperglycemia, the primary indicator of CMDs including prediabetes and type 2 diabetes mellitus (T2DM), leads to overproduction of reactive oxygen species (ROS) and oxidative stress (OxS). This condition, resulting from chronic hyperglycemia and insufficient antioxidant defense, causes damage to biomolecules, triggering diabetes complications. Additionally, aging itself can serve as a source of OxS due to the weakening of antioxidant defense mechanisms. Notably, previous research indicates that miR-196a, by downregulating glutathione peroxidase 3 (GPx3), contributes to insulin resistance (IR). Additionally, a GPx3 decrease is observed in overweight/obese and insulin-resistant individuals and in the elderly population. This study investigates plasma GPx3 levels and miR-196a expression as potential CMD risk indicators. We used ELISA to measure GPx3 and qRT-PCR for miR-196a expression, supplemented by multivariate linear regression and receiver operating characteristic (ROC) analysis. Our findings included a significant GPx3 reduction in the CMD patients (n = 126), especially in the T2DM patients (n = 51), and a decreasing trend in the prediabetes group (n = 37). miR-196a expression, although higher in the CMD and T2DM groups than in the controls, was not statistically significant, potentially due to the small sample size. In the individuals with CMD, GPx3 levels exhibited a negative correlation with the mass of adipose tissue, muscle, and total body water, while miR-196a positively correlated with fat mass. In the CMD group, the analysis revealed a weak negative correlation between glucose and GPx3 levels. ROC analysis indicated a 5.2-fold increased CMD risk with GPx3 below 419.501 ng/mL. Logistic regression suggested that each 100 ng/mL GPx3 increase corresponded to a roughly 20% lower CMD risk (OR = 0.998; 95% CI: 0.996–0.999; p = 0.031). These results support the potential of GPx3 as a biomarker for CMD, particularly in T2DM, and the lack of a significant decline in GPx3 levels in prediabetic individuals suggests that it may not serve reliably as an early indicator of CMDs, warranting further large-scale validation. Full article
(This article belongs to the Special Issue Current Research on Diabetes and Metabolic Syndrome)
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11 pages, 502 KiB  
Article
Circulating Interleukins-33 and -37 and Their Associations with Metabolic Syndrome in Arab Adults
by Osama E. Amer, Shaun Sabico, Malak N. K. Khattak, Abdullah M. Alnaami, Gamal M. Saadawy and Nasser M. Al-Daghri
Int. J. Mol. Sci. 2024, 25(2), 699; https://doi.org/10.3390/ijms25020699 - 5 Jan 2024
Viewed by 1329
Abstract
Interleukins (ILs) are a group of cytokines known to have immunomodulatory effects; they include ILs–33 and –37 whose emerging roles in the pathogenesis of metabolic syndrome (MetS) remain under investigated. In this study, we compared circulating IL–33 and IL–37 in Arab adults with [...] Read more.
Interleukins (ILs) are a group of cytokines known to have immunomodulatory effects; they include ILs–33 and –37 whose emerging roles in the pathogenesis of metabolic syndrome (MetS) remain under investigated. In this study, we compared circulating IL–33 and IL–37 in Arab adults with and without MetS to determine its associations with MetS components. A total of 417 Saudi participants (151 males, 266 females; mean age ± SD 41.3 ± 9.0 years; mean body mass index ± SD 30.7 ± 6.3 kg/m2) were enrolled and screened for MetS using the ATP III criteria. Anthropometrics and fasting blood samples were taken for the assessment of fasting glucose and lipids. Circulating levels of IL–33 and IL–37 were measured using commercially available assays. The results showed higher levels of serum IL–33 and IL–37 in participants with MetS than those without (IL-33, 3.34 3.42 (2.3–3.9) vs. (1–3.9), p = 0.057; IL-37, 5.1 (2.2–8.3) vs. 2.9 (2.1–6.1), p = 0.01). Additionally, having elevated levels of IL–33 was a risk factor for hypertension, low HDL-c, and hypertriglyceridemia. A stratification of the participants according to sex showed that males had higher IL-33 levels than females [3.7 (3.0–4.1) vs. 3.15 (1.4–3.8), p < 0.001], while females had higher levels of IL–37 than males [3.01 (2.2–7.0) vs. 2.9 (2.1–5.6), p = 0.06]. In conclusion, the presence of MetS substantially alters the expression of ILs–33 and -37. IL-33 in particular can be potentially used as a therapeutic target to prevent MetS progression. Longitudinal and interventional studies are warranted to confirm present findings. Full article
(This article belongs to the Special Issue Current Research on Diabetes and Metabolic Syndrome)
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Review

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19 pages, 1130 KiB  
Review
Metabolic Crossroads: Unveiling the Complex Interactions between Obstructive Sleep Apnoea and Metabolic Syndrome
by Aisling Heffernan, Darko Duplancic, Marko Kumric, Tina Ticinovic Kurir and Josko Bozic
Int. J. Mol. Sci. 2024, 25(6), 3243; https://doi.org/10.3390/ijms25063243 - 13 Mar 2024
Cited by 4 | Viewed by 2355
Abstract
Obstructive sleep apnoea (OSA) and components of metabolic syndrome (MetS) are inextricably connected. Considering the increasing burden of MetS and OSA, in the present review, we aimed to collate and summarise the potential pathophysiological mechanisms linking these pathologies. In short, obesity appears to [...] Read more.
Obstructive sleep apnoea (OSA) and components of metabolic syndrome (MetS) are inextricably connected. Considering the increasing burden of MetS and OSA, in the present review, we aimed to collate and summarise the potential pathophysiological mechanisms linking these pathologies. In short, obesity appears to promote OSA development via multiple pathways, some of which are not directly related to mass but rather to metabolic complications of obesity. Simultaneously, OSA promotes weight gain through central mechanisms. On the other hand, diabetes mellitus contributes to OSA pathophysiology mainly through effects on peripheral nerves and carotid body desensitization, while intermittent hypoxia and sleep fragmentation are the principal culprits in OSA-mediated diabetes. Apart from a bidirectional pathophysiological relationship, obesity and diabetes mellitus together additively increase cardiovascular risk in OSA patients. Additionally, the emergence of new drugs targeting obesity and unequivocal results of the available studies underscore the need for further exploration of the mechanisms linking MetS and OSA, all with the aim of improving outcomes in these patients. Full article
(This article belongs to the Special Issue Current Research on Diabetes and Metabolic Syndrome)
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