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Molecular Pharmacology in Diabetes
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Molecular Pharmacology in Diabetes

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 16087

Special Issue Editors

Dr. Rosa Fernandes

E-Mail Website
Guest Editor
Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: diabetic retinopathy; neuroinflammation; therapeutics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Flávio Reis

E-Mail Website
Guest Editor
1. Centre for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, 3004-504 Coimbra, Portugal
2. Institute of Pharmacology & Experimental Therapeutics & Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal
Interests: gut microbiota; therapeutics & nutraceuticals; cardiovascular & metabolic disorders; renal diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Diabetes is one of the most significant global public health concerns. Poorly controlled diabetes can have severe repercussions in a wide range of organs and tissues of the body, ranging from vascular complications, including retinopathy, nephropathy, and cardiomyopathy, to other diseases such as cancer or neurodegenerative problems. Despite advances in therapeutic strategies to lower glucose levels, some of the complications of diabetes are neither reversible nor preventable. Understanding the molecular signaling pathways underlying diabetes and related complications helps to identify potential new therapeutic targets for the management of those diseases.

This Special Issue invites important and novel advances made on the identification of key molecules and molecular signaling pathways associated with oxidative stress and inflammation in diabetes and related complications that could open up new therapeutic avenues. In addition, state-of-the-art molecular studies on therapeutical options for those diseases are also welcomed, including pre-clinical studies using relevant cellular and animal models, but excluding pure clinic-related research.

Dr. Rosa Fernandes
Dr. Flávio Reis
Guest Editors

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
  • vascular complications
  • cancer
  • neurodegenerative disorders
  • key molecular players
  • signaling pathways
  • molecular biomarkers
  • pharmacological agents
  • antioxidants
  • anti-inflammatory agents

Published Papers (7 papers)

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Editorial

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4 pages, 197 KiB  
Editorial
Molecular Pharmacology in Diabetes
by Flávio Reis and Rosa Fernandes
Int. J. Mol. Sci. 2024, 25(5), 3051; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25053051 - 06 Mar 2024
Viewed by 450
Abstract
This Special Issue highlights the key molecules and molecular signaling pathways associated with diabetes and its multifaceted complications [...] Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)

Research

Jump to: Editorial, Review

15 pages, 3507 KiB  
Article
Renoprotective Impacts of Inonotus obliquus Ethanol-Ethyl Acetate Extract on Combined Streptozotocin and Unilateral Nephrectomy-Induced Diabetic Nephropathy in Mice
by Kuang-Hsing Chiang, Yi-Chun Chiu, Noi Yar, Yu-Chun Chen, Chia-Hui Cheng, Yi-Chien Liu, Chia-Yu Chang and Jiunn-Jye Chuu
Int. J. Mol. Sci. 2023, 24(5), 4443; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054443 - 23 Feb 2023
Cited by 2 | Viewed by 3217
Abstract
Diabetes nephropathy (DN) is one of the most common causes of end stage renal disease (ESRD) globally. Medication options to stop or slow the progression of chronic renal disease (CKD) are limited, and patients with DN remain at a high risk of developing [...] Read more.
Diabetes nephropathy (DN) is one of the most common causes of end stage renal disease (ESRD) globally. Medication options to stop or slow the progression of chronic renal disease (CKD) are limited, and patients with DN remain at a high risk of developing renal failure. Inonotus obliquus extracts (IOEs) of Chaga mushroom have been shown to have anti-glycemic, anti-hyperlipidemia, antioxidant, and anti-inflammatory effects against diabetes. In this study, we examined the potential renal protective role of an ethyl acetate layer after water-ethyl acetate separation from Inonotus obliquus ethanol crude extract (EtCE-EA) from Chaga mushrooms in diabetic nephropathy mice after preparation with 1/3 NT + STZ. Our data showed that treatment with EtCE-EA can effectively regulate blood glucose, albumin-creatinine ratio, serum creatinine, and blood urea nitrogen (BUN) levels, and it can improve the renal damage in 1/3 NT + STZ-induced CRF mice with an increase in concentration (100, 300, and 500 mg/kg). In the immunohistochemical staining test, EtCE-EA can effectively reduce the expression of TGF-β and α-SMA after induction according to the increase in the concentration (100 mg/kg, 300 mg/kg), thereby slowing down the degree of kidney damage. Our findings demonstrate that EtCE-EA could provide renal protection in diabetes nephropathy, possibly due to the decreased expression of transforming growth factor-β1 and α-smooth muscle actin. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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19 pages, 4110 KiB  
Article
Circulating Dopamine Is Regulated by Dietary Glucose and Controls Glucagon-like 1 Peptide Action in White Adipose Tissue
by Gabriela Tavares, Daniela Rosendo-Silva, Flávia Simões, Hans Eickhoff, Daniela Marques, Joana F. Sacramento, Adriana M. Capucho, Raquel Seiça, Sílvia V. Conde and Paulo Matafome
Int. J. Mol. Sci. 2023, 24(3), 2464; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032464 - 27 Jan 2023
Cited by 3 | Viewed by 2358
Abstract
Dopamine directly acts in the liver and white adipose tissue (WAT) to regulate insulin signaling, glucose uptake, and catabolic activity. Given that dopamine is secreted by the gut and regulates insulin secretion in the pancreas, we aimed to determine its regulation by nutritional [...] Read more.
Dopamine directly acts in the liver and white adipose tissue (WAT) to regulate insulin signaling, glucose uptake, and catabolic activity. Given that dopamine is secreted by the gut and regulates insulin secretion in the pancreas, we aimed to determine its regulation by nutritional cues and its role in regulating glucagon-like peptide 1 (GLP-1) action in WAT. Solutions with different nutrients were administered to Wistar rats and postprandial dopamine levels showed elevations following a mixed meal and glucose intake. In high-fat diet-fed diabetic Goto-Kakizaki rats, sleeve gastrectomy upregulated dopaminergic machinery, showing the role of the gut in dopamine signaling in WAT. Bromocriptine treatment in the same model increased GLP-1R in WAT, showing the role of dopamine in regulating GLP-1R. By contrast, treatment with the GLP-1 receptor agonist Liraglutide had no impact on dopamine receptors. GLP-1 and dopamine crosstalk was shown in rat WAT explants, since dopamine upregulated GLP-1-induced AMPK activity in mesenteric WAT in the presence of the D2R and D3R inhibitor Domperidone. In human WAT, dopamine receptor 1 (D1DR) and GLP-1R expression were correlated. Our results point out a dietary and gut regulation of plasma dopamine, acting in the WAT to regulate GLP-1 action. Together with the known dopamine action in the pancreas, such results may identify new therapeutic opportunities to improve metabolic control in metabolic disorders. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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18 pages, 9963 KiB  
Article
Improvement of Glycaemia and Endothelial Function by a New Low-Dose Curcuminoid in an Animal Model of Type 2 Diabetes
by Sara Oliveira, Tamaeh Monteiro-Alfredo, Rita Henriques, Carlos Fontes Ribeiro, Raquel Seiça, Teresa Cruz, Célia Cabral, Rosa Fernandes, Fátima Piedade, Maria Paula Robalo, Paulo Matafome and Sónia Silva
Int. J. Mol. Sci. 2022, 23(10), 5652; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105652 - 18 May 2022
Cited by 4 | Viewed by 1920
Abstract
Curcumin has been suggested as a promising treatment for metabolic diseases, but the high doses required limit its therapeutic use. In this study, a new curcuminoid is synthesised to increase curcumin anti-inflammatory and antioxidant potential and to achieve hypoglycaemic and protective vascular effects [...] Read more.
Curcumin has been suggested as a promising treatment for metabolic diseases, but the high doses required limit its therapeutic use. In this study, a new curcuminoid is synthesised to increase curcumin anti-inflammatory and antioxidant potential and to achieve hypoglycaemic and protective vascular effects in type 2 diabetic rats in a lower dose. In vitro, the anti-inflammatory effect was determined through the Griess reaction, and the antioxidant activity through ABTS and TBARS assays. In vivo, Goto-Kakizaki rats were treated for 2 weeks with the equimolar dose of curcumin (40 mg/kg/day) or curcuminoid (52.4 mg/kg/day). Fasting glycaemia, insulin tolerance, plasma insulin, insulin signalling, serum FFA, endothelial function and several markers of oxidative stress were evaluated. Both compounds presented a significant anti-inflammatory effect. Moreover, the curcuminoid had a marked hypoglycaemic effect, accompanied by higher GLUT4 levels in adipose tissue. Both compounds increased NO-dependent vasorelaxation, but only the curcuminoid exacerbated the response to ascorbic acid, consistent with a higher decrease in vascular oxidative and nitrosative stress. SOD1 and GLO1 levels were increased in EAT and heart, respectively. Altogether, these data suggest that the curcuminoid developed here has more pronounced effects than curcumin in low doses, improving the oxidative stress, endothelial function and glycaemic profile in type 2 diabetes. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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Review

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16 pages, 1595 KiB  
Review
Glycosphingolipids in Diabetes, Oxidative Stress, and Cardiovascular Disease: Prevention in Experimental Animal Models
by Amrita Balram, Spriha Thapa and Subroto Chatterjee
Int. J. Mol. Sci. 2022, 23(23), 15442; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232315442 - 06 Dec 2022
Cited by 7 | Viewed by 2070
Abstract
Diabetes contributes to about 30% morbidity and mortality world-wide and has tidal wave increases in several countries in Asia. Diabetes is a multi-factorial disease compounded by inflammation, dyslipidemia, atherosclerosis, and is sometimes accompanied with gains in body weight. Sphingolipid pathways that interplay in [...] Read more.
Diabetes contributes to about 30% morbidity and mortality world-wide and has tidal wave increases in several countries in Asia. Diabetes is a multi-factorial disease compounded by inflammation, dyslipidemia, atherosclerosis, and is sometimes accompanied with gains in body weight. Sphingolipid pathways that interplay in the enhancement of the pathology of this disease may be potential therapeutic targets. Thus, the application of advanced sphingolipidomics may help predict the progression of this disease and therapeutic outcomes in man. Pre-clinical studies using various experimental animal models of diabetes provide valuable information on the role of sphingolipid signaling networks in diabetes and the efficacy of drugs to determine the translatability of innovative discoveries to man. In this review, we discuss three major concepts regarding sphingolipids and diabetes. First, we discuss a possible involvement of a monosialodihexosylceramide (GM3) in insulin–insulin receptor interactions. Second, a potential role for ceramide (Cer) and lactosylceramide (LacCer) in apoptosis and mitochondrial dysfunction is proposed. Third, a larger role of LacCer in antioxidant status and inflammation is discussed. We also discuss how inhibitors of glycosphingolipid synthesis can ameliorate diabetes in experimental animal models. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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17 pages, 1320 KiB  
Review
Heme Oxygenase-1 as Therapeutic Target for Diabetic Foot Ulcers
by Ermelindo Carreira Leal and Eugenia Carvalho
Int. J. Mol. Sci. 2022, 23(19), 12043; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231912043 - 10 Oct 2022
Cited by 11 | Viewed by 3156
Abstract
A diabetic foot ulcer (DFU) is one of the major complications of diabetes. Wound healing under diabetic conditions is often impaired. This is in part due to the excessive oxidative stress, prolonged inflammation, immune cell dysfunction, delayed re-epithelialization, and decreased angiogenesis present at [...] Read more.
A diabetic foot ulcer (DFU) is one of the major complications of diabetes. Wound healing under diabetic conditions is often impaired. This is in part due to the excessive oxidative stress, prolonged inflammation, immune cell dysfunction, delayed re-epithelialization, and decreased angiogenesis present at the wound site. As a result of these multifactorial impaired healing pathways, it has been difficult to develop effective therapeutic strategies for DFU. Heme oxygenase-1 (HO-1) is the rate-limiting enzyme in heme degradation generating carbon monoxide (CO), biliverdin (BV) which is converted into bilirubin (BR), and iron. HO-1 is a potent antioxidant. It can act as an anti-inflammatory, proliferative, angiogenic and cytoprotective enzyme. Due to its biological functions, HO-1 plays a very important role in wound healing, in part mediated through the biologically active end products generated by its enzymatic activity, particularly CO, BV, and BR. Therapeutic strategies involving the activation of HO-1, or the topical application of its biologically active end products are important in diabetic wound healing. Therefore, HO-1 is an attractive therapeutic target for DFU treatment. This review will provide an overview and discussion of the importance of HO-1 as a therapeutic target for diabetic wound healing. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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14 pages, 798 KiB  
Review
11β-HSD as a New Target in Pharmacotherapy of Metabolic Diseases
by Daria Kupczyk, Rafał Bilski, Mariusz Kozakiewicz, Renata Studzińska, Kornelia Kędziora-Kornatowska, Tomasz Kosmalski, Agnieszka Pedrycz-Wieczorska and Mariola Głowacka
Int. J. Mol. Sci. 2022, 23(16), 8984; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23168984 - 11 Aug 2022
Cited by 9 | Viewed by 1840
Abstract
Glucocorticoids (GCs), which are secreted by the adrenal cortex, are important regulators in the metabolism of carbohydrates, lipids, and proteins. For the proper functioning of the body, strict control of their release is necessary, as increased GCs levels may contribute to the development [...] Read more.
Glucocorticoids (GCs), which are secreted by the adrenal cortex, are important regulators in the metabolism of carbohydrates, lipids, and proteins. For the proper functioning of the body, strict control of their release is necessary, as increased GCs levels may contribute to the development of obesity, type 2 diabetes mellitus, hypertension, cardiovascular diseases, and other pathological conditions contributing to the development of metabolic syndrome. 11β-hydroxysteroid dehydrogenase type I (11β-HSD1) locally controls the availability of the active glucocorticoid, namely cortisol and corticosterone, for the glucocorticoid receptor. Therefore, the participation of 11β-HSD1 in the development of metabolic diseases makes both this enzyme and its inhibitors attractive targets in the pharmacotherapy of the above-mentioned diseases. Full article
(This article belongs to the Special Issue Molecular Pharmacology in Diabetes)
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