Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 5580

Special Issue Editor


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Guest Editor
Division of Nephrology, Saint Louis University, St Louis, MO, USA
Interests: diabetic kidney disease; glomerulonephritis; kidney disease; biomarkers; cardiovascular risks

Special Issue Information

Dear Colleagues,

The Special Issue “Diabetes Complications: From Pathophysiology to Novel Therapeutic Approaches 2.0” will focus on the molecular pathophysiology of diabetes mellitus and its devastating complications, as well as new biomarkers for early detection, and novel therapeutic approaches.

Diabetes mellitus has become an epidemic in recent decades. Worldwide, the data show a near quadrupling of the number of cases of diagnosed diabetes, from 108 million persons in 1980 to 425 million in 2017. There is a projected increase in the prevalence of diabetes up to 592 million (10.1%) by 2035. This increase mirrors the increasing prevalence of obesity in children and young adults, particularly those in highly susceptible ethnic groups. The long-term complications of T2DM cause a wide range of increasingly prevalent debilitating co-morbidities with complex pathophysiology in diabetic patients. Although the heritability of type 2 diabetes is high (30–70%) and more than 60 genetic variants related with diabetes risk have now been identified, the individual effects of genetic variants are modest, and even when combined into a genetic score, known genes contribute little to the prediction of diabetes. A more comprehensive understanding of the underlying molecular processes and the identification of key molecules could lead to a more precisely targeted intervention either for prevention or for treatment. Monitoring changes in the global gene expression profile, refined by global microRNA expression profiling, could provide the necessary clues to find these key components and biomarkers. This Special Issue invites original articles and reviews in basic, clinical, translational, and multidisciplinary research, including, but not limited to, the following diabetes-related topics:

  • Cardiovascular disease;
  • Hyperlipidemia;
  • Neuropathy;
  • Erectile dysfunction;
  • Nephropathy;
  • Retinopathy;
  • Skin conditions;
  • Impaired wound healing;
  • Hearing impairment;
  • Psychological effects.

Dr. Usama Elewa
Guest Editor

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Keywords

  • diabetes complications
  • epigenetic imprinting
  • molecular profiling
  • biomarkers
  • targeted therapy
  • glucose control
  • conventional and complementary approaches
  • stem cell damage
  • vascular damage and regeneration

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Related Special Issue

Published Papers (3 papers)

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Research

14 pages, 4640 KiB  
Article
Sympathetic Activation Promotes Sodium Glucose Co-Transporter-1 Protein Expression in Rodent Skeletal Muscle
by Jennifer R. Matthews, Lakshini Y. Herat, Markus P. Schlaich and Vance B. Matthews
Biomedicines 2024, 12(7), 1456; https://doi.org/10.3390/biomedicines12071456 - 1 Jul 2024
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Abstract
The hyperactivation of the sympathetic nervous system (SNS) is linked to obesity, hypertension, and type 2 diabetes, which are characterized by elevated norepinephrine (NE) levels. Previous research has shown increased sodium-dependent glucose cotransporter 1 (SGLT1) protein levels in kidneys of hypertensive rodents, prompting [...] Read more.
The hyperactivation of the sympathetic nervous system (SNS) is linked to obesity, hypertension, and type 2 diabetes, which are characterized by elevated norepinephrine (NE) levels. Previous research has shown increased sodium-dependent glucose cotransporter 1 (SGLT1) protein levels in kidneys of hypertensive rodents, prompting investigation into the expression of SGLT1 in various tissues, such as skeletal muscle. This study aimed to assess (i) whether skeletal muscle cells and tissue express SGLT1 and SGLT2 proteins; (ii) if NE increases SGLT1 levels in skeletal muscle cells, and (iii) whether the skeletal muscle of neurogenically hypertensive mice exhibits increased SGLT1 expression. We found that (i) skeletal muscle cells and tissue are a novel source of the SGLT2 protein and that (ii) NE significantly elevated SGLT1 levels in skeletal muscle cells. As SGLT2 inhibition (SGLT2i) with Empagliflozin increased SGLT1 levels, in vivo studies with the dual inhibitor SGLT1/2i, Sotagliflozin were warranted. The treatment of neurogenically hypertensive mice using Sotagliflozin significantly reduced blood pressure. Our findings suggest that SNS activity upregulates the therapeutic target, SGLT1, in skeletal muscle, potentially worsening cardiometabolic control. As clinical trial data suggest cardiorenal benefits from SGLT2i, future studies should aim to utilize SGLT1i by itself, which may offer a therapeutic strategy for conditions with heightened SNS activity, such as hypertension, diabetes, and obesity. Full article
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11 pages, 795 KiB  
Article
Foot Plantar Pressure Abnormalities in Near Adulthood Patients with Type 1 Diabetes
by Marta Wysocka-Mincewicz, Ewa Szczerbik, Maria Mazur, Magdalena Grabik, Małgorzata Kalinowska and Małgorzata Syczewska
Biomedicines 2023, 11(11), 2901; https://doi.org/10.3390/biomedicines11112901 - 26 Oct 2023
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Abstract
Increased ulcer risk diminishes the quality of life in diabetes. This study assessed abnormalities in foot plantar pressure distribution in adolescents with T1D to detect early signs of ulcer risk. A total of 102 T1D patients, without diabetic neuropathy, were included (mean age [...] Read more.
Increased ulcer risk diminishes the quality of life in diabetes. This study assessed abnormalities in foot plantar pressure distribution in adolescents with T1D to detect early signs of ulcer risk. A total of 102 T1D patients, without diabetic neuropathy, were included (mean age 17.8 years, mean diabetes duration 7.4 year). Pedography was captured using Novel emed. Data from the study group were compared with reference data. The study revealed a statistically significant reduced foot contact area in both feet in the entire foot and under the head of the fifth metatarsal bone and the second toe. In both feet, the peak pressure was increased under the entire foot, hindfoot, midfoot, first metatarsal head, big toe, and second toe. There was no statistically significant difference in peak pressure. The mean plantar pressure rating was statistically significantly increased in both feet across the entire sole, in the hindfoot, midfoot, and first metatarsal head. T1D patients of age near adulthood without neuropathy have increased values in mean pressure and reduced contact area, pointing to the need of monitoring and preventive measures. These results point to the need of further research and analysis which should include various risk factor such as foot anatomy, body posture, or certain metabolic factors. Full article
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12 pages, 1844 KiB  
Article
In Vitro Exposure to Glucose Alters the Expression of Phosphorylated Proteins in Platelets
by Mizuho Suzuki, Kyosuke Takeshita, Yuki Kitamura, Marie Kuribayashi, Zhenlie Huang, Gaku Ichihara, Shinji Oikawa and Sahoko Ichihara
Biomedicines 2023, 11(2), 543; https://doi.org/10.3390/biomedicines11020543 - 13 Feb 2023
Cited by 2 | Viewed by 1787
Abstract
Diabetes mellitus (DM) is a pro-thrombotic state that can potentially cause serious cardiovascular complications. Platelet hyperactivation plays an important role in these pathological processes, however there is little or no information on the effect of hyperglycemia on platelet proteins. The aim of this [...] Read more.
Diabetes mellitus (DM) is a pro-thrombotic state that can potentially cause serious cardiovascular complications. Platelet hyperactivation plays an important role in these pathological processes, however there is little or no information on the effect of hyperglycemia on platelet proteins. The aim of this study was to identify the molecular targets associated with platelet reactivity under hyperglycemia. Towards this goal, we examined the effects of the exposure of platelets to 1 and 2 h glucose (300 mg/dL) and control (vehicle and osmolality control using mannitol) on platelet proteins (n = 4 samples per group) using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) combined with MALDI-TOF/TOF tandem mass spectrometry. Two-hour exposure to glucose significantly up-regulated the expression of ATP synthase subunit beta, filamin-A, and L-lactate dehydrogenase A chain in platelets. Pro-Q Diamond staining confirmed the effect of 2 h glucose on vinculin, heat shock protein HSP 90-alpha, filamin-A, and fructose-bisphosphate aldolase A (platelet phosphorylated proteins). The identified proteins are involved in various cellular processes and functions and possibly in platelet reactivity under hyperglycemic conditions. Full article
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