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Pharmacological and Technological Advances for the Treatment of Diabetes and Other Metabolic Diseases

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 (31 January 2021) | Viewed by 21288

Special Issue Editors

Prof. Dr. Eliana B. Souto

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Guest Editor
Professor of Pharmaceutical Technology, Faculty of Pharmacy, University of Porto, 4099-002 Porto, Portugal
Interests: drug delivery; drug targeting; active pharmaceutical ingredients; volatile compounds; encapsulation
Special Issues, Collections and Topics in MDPI journals
Dr. Selma B. Souto

E-Mail
Guest Editor
General Secretary of the Portuguese Society for the Study of Obesity Affiliation: Department of Endocrinology, Hospital S. João, Porto, Portugal
Interests: Diabetes Mellitus; Thyroid; Obesity; Hypogonadism; Pituitaty diseases

Special Issue Information

Dear colleagues,

In the twenty-first century, metabolic diseases (e.g., diabetes, obesity, and metabolic syndrome) are still dealt with as serious clinical challenges as they are a major risk factor for other chronic diseases (e.g., cardiovascular disease and cancer). New pharmacological and technological breakthroughs aiming at improving the quality of life of patients and their compliance to the treatment have shown important outcomes in preclinical and clinical settings. New chemical entities, but also naturally-occurring bioactives, have been exploited as a treatment options, either in conventional drug formulations or in new drug delivery systems (e.g., nanoparticles). We invite you to participate in this Special Issue, by proposing research and/or review papers dealing with crosstalk dysregulation of key metabolic tissues and the latest pharmacological and technological advances in the diagnosis and treatment.

Prof. Dr. Eliana B. Souto
Dr. Selma B. Souto
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.

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Published Papers (3 papers)

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Research

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15 pages, 2256 KiB  
Article
Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Statin Toxicity
by Vlad F. Avram, Imen Chamkha, Eleonor Åsander-Frostner, Johannes K. Ehinger, Romulus Z. Timar, Magnus J. Hansson, Danina M. Muntean and Eskil Elmér
Int. J. Mol. Sci. 2021, 22(1), 424; https://doi.org/10.3390/ijms22010424 - 3 Jan 2021
Cited by 14 | Viewed by 4553
Abstract
Statins are the cornerstone of lipid-lowering therapy. Although generally well tolerated, statin-associated muscle symptoms (SAMS) represent the main reason for treatment discontinuation. Mitochondrial dysfunction of complex I has been implicated in the pathophysiology of SAMS. The present study proposed to assess the concentration-dependent [...] Read more.
Statins are the cornerstone of lipid-lowering therapy. Although generally well tolerated, statin-associated muscle symptoms (SAMS) represent the main reason for treatment discontinuation. Mitochondrial dysfunction of complex I has been implicated in the pathophysiology of SAMS. The present study proposed to assess the concentration-dependent ex vivo effects of three statins on mitochondrial respiration in viable human platelets and to investigate whether a cell-permeable prodrug of succinate (complex II substrate) can compensate for statin-induced mitochondrial dysfunction. Mitochondrial respiration was assessed by high-resolution respirometry in human platelets, acutely exposed to statins in the presence/absence of the prodrug NV118. Statins concentration-dependently inhibited mitochondrial respiration in both intact and permeabilized cells. Further, statins caused an increase in non-ATP generating oxygen consumption (uncoupling), severely limiting the OXPHOS coupling efficiency, a measure of the ATP generating capacity. Cerivastatin (commercially withdrawn due to muscle toxicity) displayed a similar inhibitory capacity compared with the widely prescribed and tolerable atorvastatin, but did not elicit direct complex I inhibition. NV118 increased succinate-supported mitochondrial oxygen consumption in atorvastatin/cerivastatin-exposed platelets leading to normalization of coupled (ATP generating) respiration. The results acquired in isolated human platelets were validated in a limited set of experiments using atorvastatin in HepG2 cells, reinforcing the generalizability of the findings. Full article
(This article belongs to the Special Issue Pharmacological and Technological Advances for the Treatment of Diabetes and Other Metabolic Diseases)
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Review

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13 pages, 723 KiB  
Review
Dietary and Protective Factors to Halt or Mitigate Progression of Autoimmunity, COVID-19 and Its Associated Metabolic Diseases
by Camillo Ricordi, Francesca Pacifici, Giacomo Lanzoni, Anna Teresa Palamara, Enrico Garaci and David Della-Morte
Int. J. Mol. Sci. 2021, 22(6), 3134; https://doi.org/10.3390/ijms22063134 - 19 Mar 2021
Cited by 12 | Viewed by 6735
Abstract
COVID-19 is without any doubt the worst pandemic we have faced since the H1N1 virus outbreak. Even if vaccination against SARS-CoV-2 infection is becoming increasingly available, a more feasible approach for COVID-19 prevention and therapy is still needed. Evidence of a pathological link [...] Read more.
COVID-19 is without any doubt the worst pandemic we have faced since the H1N1 virus outbreak. Even if vaccination against SARS-CoV-2 infection is becoming increasingly available, a more feasible approach for COVID-19 prevention and therapy is still needed. Evidence of a pathological link between metabolic diseases and severe forms of COVID-19 has stimulated critical reflection and new considerations. In particular, an abnormal immune response observed in certain patients with SARS-CoV-2 infection suggested possible common predisposing risk factors with autoimmune diseases such as Type 1 Diabetes (T1D). Correct supplementation with dietary factors may be key to preventing and counteracting both the underlying metabolic impairment and the complications of COVID-19. A set of agents may inhibit the cytokine storm and hypercoagulability that characterize severe COVID-19 infection: vitamin D3, omega-3 polyunsaturated fatty acids, polyphenols like pterostilbene, polydatin and honokiol, which can activate anti-inflammatory and antioxidant sirtuins pathways, quercetin, vitamin C, zinc, melatonin, lactoferrin and glutathione. These agents could be highly beneficial for subjects who have altered immune responses. In this review, we discuss the antiviral and metabolic effects of these dietary factors and propose their combination for potential applications in the prevention and treatment of COVID-19. Rigorous studies will be fundamental for validating preventive and therapeutic protocols that could be of assistance to mitigate disease progression following SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Pharmacological and Technological Advances for the Treatment of Diabetes and Other Metabolic Diseases)
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26 pages, 337 KiB  
Review
Pharmacogenetics of Type 2 Diabetes—Progress and Prospects
by Yulia A. Nasykhova, Ziravard N. Tonyan, Anastasiia A. Mikhailova, Maria M. Danilova and Andrey S. Glotov
Int. J. Mol. Sci. 2020, 21(18), 6842; https://doi.org/10.3390/ijms21186842 - 18 Sep 2020
Cited by 39 | Viewed by 9177
Abstract
Type 2 diabetes mellitus (T2D) is a chronic metabolic disease resulting from insulin resistance and progressively reduced insulin secretion, which leads to impaired glucose utilization, dyslipidemia and hyperinsulinemia and progressive pancreatic beta cell dysfunction. The incidence of type 2 diabetes mellitus is increasing [...] Read more.
Type 2 diabetes mellitus (T2D) is a chronic metabolic disease resulting from insulin resistance and progressively reduced insulin secretion, which leads to impaired glucose utilization, dyslipidemia and hyperinsulinemia and progressive pancreatic beta cell dysfunction. The incidence of type 2 diabetes mellitus is increasing worldwide and nowadays T2D already became a global epidemic. The well-known interindividual variability of T2D drug actions such as biguanides, sulfonylureas/meglitinides, DPP-4 inhibitors/GLP1R agonists and SGLT-2 inhibitors may be caused, among other things, by genetic factors. Pharmacogenetic findings may aid in identifying new drug targets and obtaining in-depth knowledge of the causes of disease and its physiological processes, thereby, providing an opportunity to elaborate an algorithm for tailor or precision treatment. The aim of this article is to summarize recent progress and discoveries for T2D pharmacogenetics and to discuss the factors which limit the furthering accumulation of genetic variability knowledge in patient response to therapy that will allow improvement the personalized treatment of T2D. Full article
(This article belongs to the Special Issue Pharmacological and Technological Advances for the Treatment of Diabetes and Other Metabolic Diseases)
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