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Molecular Therapeutics for Diabetes and Related Complications

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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: closed (30 November 2024) | Viewed by 17454

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Dr. Kota V. Ramana

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Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA
Interests: oxidative stress-induced signal transduction mechanisms; pathophysiology of secondary diabetic complications; carcinogenesis; inflammatory complications; therapeutic development of small molecular inhibitors and antioxidants
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Dear Colleagues,

Diabetes poses a significant threat to global health, demanding attention due to its escalating prevalence and associated complications. Conventional treatments, such as insulin therapy, alongside newer glucose-lowering medications such as metformin, GLP-1 receptor agonists, SGLT-2 inhibitors, and insulin sensitizers, offer some effectiveness; however, they are also associated with some unwanted side effects, which necessitates the further exploration of novel therapeutic avenues. The healthcare costs of this pathology increase every year worldwide, and there is a need to discover novel drug targets and molecular pathways for managing diabetes and its associated complications, such as diabetic nephropathy, retinopathy, neuropathy, and cardiovascular diseases. These targets not only promise to ameliorate diabetes, but also offer avenues for mitigating the associated complications. Connecting these novel pathways will help to surpass the benefits of conventional therapies, thereby reducing the morbidity and mortality linked with diabetic complications. While recent preclinical studies have identified promising molecular pathways and targets, further clinical trials are needed in order to translate these findings into clinical practice. Additionally, research is continuing to explore means of reducing oxidative stress, enhancing antioxidant status, manipulating molecular metabolic pathways using the innate immune response, and exploring microRNAs, stem cell therapy, and gene therapy as potential diagnostic and therapeutic tools. Thus, while conventional therapies remain crucial, the pursuit of novel molecular therapeutics holds promise regarding the revolutionization of diabetes management and the improvement of patient outcomes. This Special Issue aims to compile state-of-the-art insights into the role of novel molecular therapeutics in ameliorating diabetes and related complications, and welcomes the submission of original research and review articles addressing all aspects of molecular and cellular pathways, therapeutic drug development, biomarker identification and verification, novel techniques, and computational, structural, and functional studies in the field of diabetes and its complications.

Dr. Kota V. Ramana
Guest Editor

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Keywords

diabetes
diabetes complications
molecular therapeutics
drug development
hyperglycemia
insulin resistance
cell signaling and oxidative stress

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Related Special Issue

Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition in International Journal of Molecular Sciences (1 article)

Published Papers (10 papers)

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Research

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16 pages, 654 KiB

Open AccessArticle

Adiponectin C1Q and Collagen Domain Containing rs266729, Cyclin-Dependent Kinase Inhibitor 2A and 2B rs10811661, and Signal Sequence Receptor Subunit 1 rs9505118 Polymorphisms and Their Association with Gestational Diabetes Mellitus: A Case-Control Study in a Romanian Population

by Mihai Muntean, Claudiu Mărginean, Elena Silvia Bernad, Claudia Bănescu, Victoria Nyulas, Irina Elena Muntean and Vladut Săsăran

Int. J. Mol. Sci. 2025, 26(4), 1654; https://doi.org/10.3390/ijms26041654 - 14 Feb 2025

Viewed by 589

Abstract

Gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (T2DM) are public health concerns worldwide. These two diseases share the same pathophysiological and genetic similarities. This study aimed to investigate the T2DM known single nucleotide polymorphisms (SNPs) of the adiponectin C1Q and collagen domain containing (ADIPOQ), cyclin-dependent kinase inhibitor 2A and 2B (CDKN2A/2B), and signal sequence receptor subunit 1 (SSR1) genes in a cohort of Romanian GDM pregnant women and perinatal outcomes. DNA was isolated from the peripheral blood of 213 pregnant women with (n = 71) or without (n = 142) GDM. Afterward, ADIPOQ (rs266729), CDKN2A/2B (rs10811661), and SSR1 (rs9505118) gene polymorphisms were genotyped using TaqMan Real-Time PCR analysis. Women with GDM had a higher pre-pregnancy body mass index (BMI) (p < 0.0001), higher BMI (p < 0.0001), higher insulin resistance homeostatic model assessment (IR-HOMA) (p = 0.0002), higher insulin levels (p = 0.003), and lower adiponectin levels (p = 0.004) at birth compared to pregnant women with normoglycemia. GDM pregnant women had gestational hypertension (GH) more frequently during pregnancy (p < 0.0001), perineal lacerations more frequently during vaginal birth (p = 0.03), and more macrosomic newborns (p < 0.0001) than pregnant women from the control group. We did not find an association under any model (allelic, genotypic, dominant, or recessive) of ADIPOQ rs266729, CDKN2A/2B rs10811661, and SSR1 rs9505118 polymorphisms and GDM. In correlation analysis, we found a weak positive correlation (r = 0.24) between the dominant model GG + CG vs. CC of rs266729 and labor induction failure. In the dominant model TT vs. CC + CT of rs10811661, we found a weak negative correlation between this model and perineal lacerations. Our results suggest that the ADIPOQ rs266729, the CDKN2A/2B rs10811661, and the SSR1 rs9505118 gene polymorphisms are not associated with GDM in a cohort of Romanian pregnant women. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

18 pages, 7003 KiB

Open AccessArticle

Oxidative Stress and Histomorphometric Remodeling: Two Key Intestinal Features of Type 2 Diabetes in Goto–Kakizaki Rats

by Marisa Esteves-Monteiro, Mariana Ferreira-Duarte, Cláudia Vitorino-Oliveira, José Costa-Pires, Sara Oliveira, Paulo Matafome, Manuela Morato, Patrícia Dias-Pereira, Vera Marisa Costa and Margarida Duarte-Araújo

Int. J. Mol. Sci. 2024, 25(22), 12115; https://doi.org/10.3390/ijms252212115 - 12 Nov 2024

Cited by 1 | Viewed by 895

Abstract

Gastrointestinal complications of diabetes are often overlooked, despite affecting up to 75% of patients. This study innovatively explores local glutathione levels and morphometric changes in the gut of Goto–Kakizaki (GK) rats, a type 2 diabetes animal model. Segments of the intestine, cecum, and colon were collected for histopathological analysis and glutathione quantification. A significant increase in the total thickness of the intestinal wall of GK rats was observed, particularly in the duodenum (1089.02 ± 39.19 vs. 864.19 ± 37.17 µm), ileum (726.29 ± 24.75 vs. 498.76 ± 16.86 µm), cecum (642.24 ± 34.15 vs. 500.97 ± 28.81 µm), and distal colon (1211.81 ± 51.32 vs. 831.71 ± 53.2 µm). Additionally, diabetic rats exhibited thickening of the muscular layers in all segments, except for the duodenum, which was also the only portion where the number of smooth muscle cells did not decrease. Moreover, myenteric neuronal density was lower in GK rats, suggesting neurological loss. Total glutathione levels were lower in all intestinal segments of diabetic rats (except duodenum), and the reduced/oxidized glutathione ratio (GSH/GSSG) was significantly decreased in GK rats, indicating increased oxidative stress. These findings strongly indicate that GK rats undergo significant intestinal remodeling, notable shifts in neuronal populations, and heightened oxidative stress—factors that likely contribute to the functional gastrointestinal alterations seen in diabetic patients. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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10 pages, 607 KiB

Open AccessArticle

The GDF15 3′ UTR Polymorphism rs1054564 Is Associated with Diabetes and Subclinical Atherosclerosis

by Montse Guardiola, Josefa Girona, Emma Barroso, María García-Altares, Daiana Ibarretxe, Núria Plana, Josep Ribalta, Xavier Correig, Manuel Vázquez-Carrera, Lluís Masana and Ricardo Rodríguez-Calvo

Int. J. Mol. Sci. 2024, 25(22), 11985; https://doi.org/10.3390/ijms252211985 - 7 Nov 2024

Cited by 1 | Viewed by 1280

Abstract

Growth differentiation factor 15 (GDF15) is a stress-response cytokine related to a wide variety of metabolic diseases. However, the impact of GDF15-specific genetic variants on the abovementioned conditions is poorly known. The aim of this study was to assess the impact of selected GDF15 single-nucleotide polymorphisms (SNPs) on metabolic disturbances and subclinical atherosclerosis. A cross-sectional study involving 153 participants of a metabolic patient-based cohort was performed. Three selected SNPs (rs888663, rs1054564 and rs1059369) in a locus on chromosome 19 including the GDF15 gene were genotyped by Polymerase Chain Reaction (PCR), and its relationship with the serum GDF15 levels, health status and clinical variables were analyzed. Of the three SNPs analyzed, only rs1054564 showed different distributions between the healthy volunteers and patients suffering lipid alterations and associated disorders. Accordingly, just the rs1054564 variant carriers showed a significant increase in GDF15 serum levels compared to the wild-type carriers. The group of variant carriers showed a higher frequency of individuals with diabetes, compared to the wild-type carrier group, without showing differences in other metabolic conditions. Additionally, the frequency of individuals with atherosclerotic carotid plaque was higher in the rs1054564 variant carriers than in the wild-type carriers. Logistic regression models identified that the presence of the rs1054564 variant carriers increase the likelihood for both diabetes and carotid plaque independently of confounding factors. Overall, the findings of this study identify the rs1054564 variant as a potential indicator for the likelihood of diabetes and subclinical atherosclerosis. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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22 pages, 4710 KiB

Open AccessArticle

New Application of an Old Drug: Anti-Diabetic Properties of Phloroglucinol

by Krzysztof Drygalski, Mateusz Maciejczyk, Urszula Miksza, Andrzej Ustymowicz, Joanna Godzień, Angelika Buczyńska, Andrzej Chomentowski, Iga Walczak, Karolina Pietrowska, Julia Siemińska, Cezary Pawlukianiec, Przemysław Czajkowski, Joanna Fiedorczuk, Monika Moroz, Beata Modzelewska, Anna Zalewska, Barbara Kutryb-Zając, Tomasz Kleszczewski, Michał Ciborowski, Hady Razak Hady, Marc Foretz and Edyta Adamska-Patruno Show full author list Hide full author list

Int. J. Mol. Sci. 2024, 25(19), 10291; https://doi.org/10.3390/ijms251910291 - 24 Sep 2024

Cited by 1 | Viewed by 2152

Abstract

Phloroglucinol (PHG), an analgesic and spasmolytic drug, shows promise in preventing high-fat-diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) and insulin resistance. In Wistar rats, 10 weeks of PHG treatment did not prevent HFD-induced weight gain but significantly mitigated fasting hyperglycemia, impaired insulin responses, and liver steatosis. This protective effect was not linked to hepatic lipogenesis or AMP-activated protein kinase (AMPK) activation. Instead, PHG improved mitochondrial function by reducing oxidative stress, enhancing ATP production, and increasing anti-oxidant enzyme activity. PHG also relaxed gastric smooth muscles via potassium channel activation and nitric oxide (NO) signaling, potentially delaying gastric emptying. A pilot intervention in pre-diabetic men confirmed PHG’s efficacy in improving postprandial glycemic control and altering lipid metabolism. These findings suggest PHG as a potential therapeutic for NAFLD and insulin resistance, acting through mechanisms involving mitochondrial protection, anti-oxidant activity, and gastric motility modulation. Further clinical evaluation is warranted to explore PHG’s full therapeutic potential. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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11 pages, 515 KiB

Open AccessArticle

Novel Metabolites Associated with Decreased GFR in Finnish Men: A 12-Year Follow-Up of the METSIM Cohort

by Lilian Fernandes Silva, Jagadish Vangipurapu, Anniina Oravilahti and Markku Laakso

Int. J. Mol. Sci. 2024, 25(18), 10044; https://doi.org/10.3390/ijms251810044 - 18 Sep 2024

Viewed by 1027

Abstract

Identification of the individuals having impaired kidney function is essential in preventing the complications of this disease. We measured 1009 metabolites at the baseline study in 10,159 Finnish men of the METSIM cohort and associated the metabolites with an estimated glomerular filtration rate (eGFR). A total of 7090 men participated in the 12-year follow-up study. Non-targeted metabolomics profiling was performed at Metabolon, Inc. (Morrisville, NC, USA) on EDTA plasma samples obtained after overnight fasting. We applied liquid chromatography mass spectrometry (LC-MS/MS) to identify the metabolites (the Metabolon DiscoveryHD4 platform). We performed association analyses between the eGFR and metabolites using linear regression adjusted for confounding factors. We found 108 metabolites significantly associated with a decrease in eGFR, and 28 of them were novel, including 12 amino acids, 8 xenobiotics, 5 lipids, 1 nucleotide, 1 peptide, and 1 partially characterized molecule. The most significant associations were with five amino acids, N-acetylmethionine, N-acetylvaline, gamma-carboxyglutamate, 3-methylglutaryl-carnitine, and pro-line. We identified 28 novel metabolites associated with decreased eGFR in the 12-year follow-up study of the METSIM cohort. These findings provide novel insights into the role of metabolites and metabolic pathways involved in the decline of kidney function. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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Review

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35 pages, 492 KiB

Open AccessReview

Exploring the Therapeutic Potential of N-Methyl-D-Aspartate Receptor Antagonists in Neuropathic Pain Management

by Ciprian Pușcașu, Cornel Chiriță, Simona Negreș and Nicoleta Mirela Blebea

Int. J. Mol. Sci. 2024, 25(20), 11111; https://doi.org/10.3390/ijms252011111 - 16 Oct 2024

Cited by 3 | Viewed by 1996

Abstract

Neuropathic pain (NeP) is a complex and debilitating condition that impacts millions of people globally. Although various treatment options exist, their effectiveness is often limited, and they can be accompanied by significant side effects. In recent years, there has been increasing interest in targeting the N-methyl-D-aspartate receptor (NMDAR) as a potential therapeutic approach to alleviate different types of neuropathic pain. This narrative review aims to provide a comprehensive examination of NMDAR antagonists, specifically ketamine, memantine, methadone, amantadine, carbamazepine, valproic acid, phenytoin, dextromethorphan, riluzole, and levorphanol, in the management of NeP. By analyzing and summarizing current preclinical and clinical studies, this review seeks to evaluate the efficacy of these pharmacologic agents in providing adequate relief for NeP. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

20 pages, 1289 KiB

Open AccessReview

Mesenchymal Stem Cell Therapy: Therapeutic Opportunities and Challenges for Diabetic Kidney Disease

by Jia Cheng and Chun Zhang

Int. J. Mol. Sci. 2024, 25(19), 10540; https://doi.org/10.3390/ijms251910540 - 30 Sep 2024

Viewed by 2424

Abstract

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD), which severely affects the quality of patients’ lives. However, the current therapeutic approaches can only postpone its progression to ESRD. It is therefore imperative to develop a novel therapeutic strategy for renal injury in DKD, with the objective of restoring renal function and reversing the process of ESRD. In recent years, the potential of mesenchymal stem cell (MSC) therapy for DKD has garnered increasing attention within the scientific community. Preclinical research on MSC therapy has yielded promising results, and the safety of MSC treatment in vivo has been substantiated in clinical studies. An increasing body of evidence suggests that MSC therapy has significant potential for the treatment of DKD. This article reviews the existing research on MSCs and their derived exosomes in treating DKD and analyzes the underlying mechanism of MSC-based therapy for DKD. Additionally, we discuss the potential of combining MSC therapy with conventional pharmacological treatments, along with the constraints and prospects of MSC therapy for DKD. We hope this review can provide a precise and comprehensive understanding of MSCs for the treatment of DKD. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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16 pages, 3075 KiB

Open AccessReview

Endocrine-Disrupting Chemicals and the Development of Diabetes Mellitus Type 1: A 5-Year Systematic Review

by Georgia-Nektaria Keskesiadou, Sophia Tsokkou, Ioannis Konstantinidis, Maria-Nefeli Georgaki, Antonia Sioga, Theodora Papamitsou and Sofia Karachrysafi

Int. J. Mol. Sci. 2024, 25(18), 10111; https://doi.org/10.3390/ijms251810111 - 20 Sep 2024

Cited by 1 | Viewed by 2498

Abstract

Introduction: According to the Institute of Environmental Sciences, endocrine-disrupting chemicals (EDCs) are “natural or human-made chemicals that may mimic, block, or interfere with the body’s hormones, associated with a wide array of health issues”, mainly in the endocrine system. Recent studies have discussed the potential contribution of EDCs as risk factors leading to diabetes mellitus type 1 (T1DM), through various cellular and molecular pathways. Purpose: The purpose of this study was to investigate the correlation between the EDCs and the development of T1DM. Methodology: Thus, a 5-year systematic review was conducted to bring light to this research question. Using the meta-analysis and systematic review guideline protocol, a PRISMA flow diagram was constructed and, using the keywords (diabetes mellitus type 1) AND (endocrine-disrupting chemicals) in the databases PubMed, Scopus and ScienceDirect, the relevant data was collected and extracted into tables. Quality assessment tools were employed to evaluate the quality of the content of each article retrieved. Results: Based on the data collected and extracted from both human and animal studies, an association was found between T1DM and certain EDCs, such as bisphenol A (BPA), bisphenol S (BPS), persistent organic pollutants (POPs), phthalates and dioxins. Moreover, based on the quality assessments performed, using the Newcastle–Ottawa Scale and ARRIVE quality assessment tool, the articles were considered of high quality and thus eligible to justify the correlation of the EDCs and the development of T1DM. Conclusion: Based on the above study, the correlation can be justified; however, additional studies can be made focusing mainly on humans to understand further the pathophysiologic mechanism involved in this association. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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19 pages, 755 KiB

Open AccessReview

Molecular Therapeutics for Diabetic Kidney Disease: An Update

by Man Guo, Fangfang He and Chun Zhang

Int. J. Mol. Sci. 2024, 25(18), 10051; https://doi.org/10.3390/ijms251810051 - 19 Sep 2024

Cited by 1 | Viewed by 3019

Abstract

Diabetic kidney disease (DKD) is a common microvascular complication of diabetes mellitus (DM). With the increasing prevalence of DM worldwide, the incidence of DKD remains high. If DKD is not well controlled, it can develop into chronic kidney disease or end-stage renal disease (ESRD), which places considerable economic pressure on society. Traditional therapies, including glycemic control, blood pressure control, blood lipid control, the use of renin–angiotensin system blockers and novel drugs, such as sodium–glucose cotransporter 2 inhibitors, mineralocorticoid receptor inhibitors and glucagon-like peptide-1 receptor agonists, have been used in DKD patients. Although the above treatment strategies can delay the progression of DKD, most DKD patients still ultimately progress to ESRD. Therefore, new and multimodal treatment methods need to be explored. In recent years, researchers have continuously developed new treatment methods and targets to delay the progression of DKD, including miRNA therapy, stem cell therapy, gene therapy, gut microbiota-targeted therapy and lifestyle intervention. These new molecular therapy methods constitute opportunities to better understand and treat DKD. In this review, we summarize the progress of molecular therapeutics for DKD, leading to new treatment strategies. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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9 pages, 676 KiB

Open AccessCase Report

Carnitine Deficiency Caused by Salcaprozic Acid Sodium Contained in Oral Semaglutide in a Patient with Multiple Acyl-CoA Dehydrogenase Deficiency

by Yasuko Mikami-Saito, Masamitsu Maekawa, Masahiro Watanabe, Shinichiro Hosaka, Kei Takahashi, Eriko Totsune, Natsuko Arai-Ichinoi, Atsuo Kikuchi, Shigeo Kure, Hideki Katagiri and Yoichi Wada

Int. J. Mol. Sci. 2025, 26(7), 2962; https://doi.org/10.3390/ijms26072962 - 25 Mar 2025

Viewed by 502

Abstract

Carnitine plays an essential role in maintaining energy homeostasis and metabolic flexibility. Various medications, such as pivalate-conjugated antibiotics, valproic acid, and anticancer agents, can induce carnitine deficiency, inhibit the utilization of fatty acid, and contribute to the development of hypoglycemia. No studies have linked oral semaglutide to carnitine deficiency. Herein, we report the case of a 34-year-old male patient with multiple acyl-CoA dehydrogenase deficiency who developed carnitine deficiency attributable to salcaprozic acid sodium (SNAC) in oral semaglutide. The patient was diagnosed with type 2 diabetes mellitus at 32 years of age and was treated with semaglutide injections. Hypoglycemic symptoms appeared after switching to oral semaglutide, and the mean levels of blood-free carnitine significantly decreased. Liquid chromatography–tandem mass spectrometry analysis revealed a peak corresponding to the SNAC–carnitine complex (m/z 423.24) in the urine exclusively during the oral administration of semaglutide. The MS/MS spectra at m/z 423.24 contained peaks consistent with those of the SNAC and carnitine product ions. Our results suggest that through complexation with carnitine, SNAC may induce carnitine deficiency. Healthcare providers should monitor for carnitine deficiency when administering SNAC-containing medications to at-risk individuals. Furthermore, this case can raise more significant concerns about the potential impact of pharmaceutical excipients like SNAC on metabolic pathways. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications)

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