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Molecular Pharmacology of Human Metabolism Diseases
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Molecular Pharmacology of Human Metabolism Diseases

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 (20 February 2025) | Viewed by 7074

Special Issue Editor

Dr. Lukasz Buldak

E-Mail Website
Guest Editor
Department of Internal Medicine and Clinical Pharmacology, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Medyków 18, 40-752 Katowice, Poland
Interests: internal medicine; endocrinology; clinical pharmacology; obesity; metabolic diseases; hyperlipidemia; diabetes; arterial hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic diseases are gaining more and more attention due to the widespread occurrence of obesity leading to acquired lipid and glucose metabolism abnormalities, thus resulting in elevated cardiovascular risk. However, it is crucial to note that there are also severe but less common metabolic diseases resulting from specific mutations (e.g., storage disorders) that lead to disabilities. Great improvements in molecular diagnostics have enabled researchers to pinpoint pathological pathways involved in the pathogenesis of the disease. In some cases, it has led to the introduction of therapeutic measures, but many still need to be addressed.

Therefore, this Special Issue focuses on the exploration of the pathophysiological background of both common and rare metabolic disease. Novel data, including research papers as well as review articles, on potential therapeutic targets, experimental therapeutic approaches and clinical experience with novel drugs are welcome.

Dr. Lukasz Buldak
Guest Editor

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

  • metabolic diseases
  • storage disorders
  • diabetes
  • hyperlipidemia
  • inherited diseases
  • obesity
  • fatty liver
  • genetic disorder
  • pharmacotherapy

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Published Papers (4 papers)

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Research

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16 pages, 3684 KiB  
Article
Honokiol and Nicotinamide Adenine Dinucleotide Improve Exercise Endurance in Pulmonary Hypertensive Rats Through Increasing SIRT3 Function in Skeletal Muscle
by Min Li, Brittany Alexandre McKeon, Sue Gu, Ram Raj Prasad, Hui Zhang, Sushil Kumar, Suzette Riddle, David C. Irwin and Kurt R. Stenmark
Int. J. Mol. Sci. 2024, 25(21), 11600; https://doi.org/10.3390/ijms252111600 - 29 Oct 2024
Viewed by 1040
Abstract
Pulmonary hypertension (PH) significantly impairs exercise capacity and the quality of life in patients, which is influenced by dysfunctions in multiple organ systems, including the right ventricle, lungs, and skeletal muscles. Recent research has identified metabolic reprogramming and mitochondrial dysfunction as contributing factors [...] Read more.
Pulmonary hypertension (PH) significantly impairs exercise capacity and the quality of life in patients, which is influenced by dysfunctions in multiple organ systems, including the right ventricle, lungs, and skeletal muscles. Recent research has identified metabolic reprogramming and mitochondrial dysfunction as contributing factors to reduced exercise tolerance in PH patients. In this study, we investigated the therapeutic potential of enhancing mitochondrial function through the activation of the mitochondrial deacetylase SIRT3, using SIRT3 activator Honokiol combined with the SIRT3 co-factor nicotinamide adenine dinucleotide (NAD), in a Sugen/Hypoxia-induced PH rat model. Our results show that Sugen/Hypoxia-induced PH significantly impairs RV, lung, and skeletal muscle function, leading to reduced exercise capacity. Treatment with Honokiol and NAD notably improved exercise endurance, primarily by restoring SIRT3 levels in skeletal muscles, reducing proteolysis and atrophy in the gastrocnemius, and enhancing mitochondrial complex I levels in the soleus. These effects were independent of changes in cardiopulmonary hemodynamics. We concluded that targeting skeletal muscle dysfunction may be a promising approach to improving exercise capacity and overall quality of life in PH patients. Full article
(This article belongs to the Special Issue Molecular Pharmacology of Human Metabolism Diseases)
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27 pages, 6553 KiB  
Article
Aripiprazole, but Not Olanzapine, Alters the Response to Oxidative Stress in Fao Cells by Reducing the Activation of Mitogen-Activated Protein Kinases (MAPKs) and Promoting Cell Survival
by Barbara Kramar, Tinkara Pirc Marolt, Ayse Mine Yilmaz Goler, Dušan Šuput, Irina Milisav and María Monsalve
Int. J. Mol. Sci. 2024, 25(20), 11119; https://doi.org/10.3390/ijms252011119 - 16 Oct 2024
Cited by 1 | Viewed by 1604
Abstract
Prolonged use of atypical antipsychotics (AAPs) is commonly associated with increased cardiovascular disease risk. While weight gain and related health issues are generally considered the primary contributors to this risk, direct interference with mitochondrial bioenergetics, particularly in the liver where these drugs are [...] Read more.
Prolonged use of atypical antipsychotics (AAPs) is commonly associated with increased cardiovascular disease risk. While weight gain and related health issues are generally considered the primary contributors to this risk, direct interference with mitochondrial bioenergetics, particularly in the liver where these drugs are metabolized, is emerging as an additional contributing factor. Here, we compared the effects of two AAPs with disparate metabolic profiles on the response of Fao hepatoma cells to oxidative stress: olanzapine (OLA), which is obesogenic, and aripiprazole (ARI), which is not. Results showed that cells treated with ARI exhibited resistance to H2O2-induced oxidative stress, while OLA treatment had the opposite effect. Despite enhanced survival, ARI-treated cells exhibited higher apoptotic rates than OLA-treated cells when exposed to H2O2. Gene expression analysis of pro- and anti-apoptotic factors revealed that ARI-treated cells had a generally blunted response to H2O2, contrasting with a heightened response in OLA-treated cells. This was further supported by the reduced activation of MAPKs and STAT3 in ARI-treated cells in response to H2O2, whereas OLA pre-treatment enhanced their activation. The loss of stress response in ARI-treated cells was consistent with the observed increase in the mitochondrial production of O2•-, a known desensitizing factor. The physiological relevance of O2•- in ARI-treated cells was demonstrated by the increase in mitophagy flux, likely related to mitochondrial damage. Notably, OLA treatment protected proteasome activity in Fao cells exposed to H2O2, possibly due to the better preservation of stress signaling and mitochondrial function. In conclusion, this study highlights the underlying changes in cell physiology and mitochondrial function by AAPs. ARI de-sensitizes Fao cells to stress signaling, while OLA has the opposite effect. These findings contribute to our understanding of the metabolic risks associated with prolonged AAP use and may inform future therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Pharmacology of Human Metabolism Diseases)
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14 pages, 2369 KiB  
Article
Effect of mTORC Agonism via MHY1485 with and without Rapamycin on C2C12 Myotube Metabolism
by Norah E. Cook, Macey R. McGovern, Toheed Zaman, Pamela M. Lundin and Roger A. Vaughan
Int. J. Mol. Sci. 2024, 25(13), 6819; https://doi.org/10.3390/ijms25136819 - 21 Jun 2024
Viewed by 1624
Abstract
The mechanistic target of rapamycin complex (mTORC) regulates protein synthesis and can be activated by branched-chain amino acids (BCAAs). mTORC has also been implicated in the regulation of mitochondrial metabolism and BCAA catabolism. Some speculate that mTORC overactivation by BCAAs may contribute to [...] Read more.
The mechanistic target of rapamycin complex (mTORC) regulates protein synthesis and can be activated by branched-chain amino acids (BCAAs). mTORC has also been implicated in the regulation of mitochondrial metabolism and BCAA catabolism. Some speculate that mTORC overactivation by BCAAs may contribute to insulin resistance. The present experiments assessed the effect of mTORC activation on myotube metabolism and insulin sensitivity using the mTORC agonist MHY1485, which does not share structural similarities with BCAAs. Methods: C2C12 myotubes were treated with MHY1485 or DMSO control both with and without rapamycin. Gene expression was assessed using qRT-PCR and insulin sensitivity and protein expression by western blot. Glycolytic and mitochondrial metabolism were measured by extracellular acidification rate and oxygen consumption. Mitochondrial and lipid content were analyzed by fluorescent staining. Liquid chromatography-mass spectrometry was used to assess extracellular BCAAs. Results: Rapamycin reduced p-mTORC expression, mitochondrial content, and mitochondrial function. Surprisingly, MHY1485 did not alter p-mTORC expression or cell metabolism. Neither treatment altered indicators of BCAA metabolism or extracellular BCAA content. Conclusion: Collectively, inhibition of mTORC via rapamycin reduces myotube metabolism and mitochondrial content but not BCAA metabolism. The lack of p-mTORC activation by MHY1485 is a limitation of these experiments and warrants additional investigation. Full article
(This article belongs to the Special Issue Molecular Pharmacology of Human Metabolism Diseases)
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Review

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19 pages, 3344 KiB  
Review
Efficacy and Safety of Agomelatine in Depressed Patients with Diabetes: A Systematic Review and Meta-Analysis
by Adam Gędek, Szymon Modrzejewski, Michał Materna, Zofia Szular, Adam Wichniak, Paweł Mierzejewski and Monika Dominiak
Int. J. Mol. Sci. 2024, 25(23), 12631; https://doi.org/10.3390/ijms252312631 - 25 Nov 2024
Viewed by 2007
Abstract
Major depressive disorder (MDD) and diabetes mellitus (DM) remain among the most prevalent diseases and the most significant challenges faced by medicine in the 21st century. The frequent co-occurrence and bidirectional relationship between the two conditions necessitates the identification of treatment strategies that [...] Read more.
Major depressive disorder (MDD) and diabetes mellitus (DM) remain among the most prevalent diseases and the most significant challenges faced by medicine in the 21st century. The frequent co-occurrence and bidirectional relationship between the two conditions necessitates the identification of treatment strategies that benefit both. The purpose of this study was to systematically review and meta-analyze data on the efficacy and safety of agomelatine (AGO) in the treatment of patients with depression with comorbid diabetes to explore its potential mechanism of action in both diseases and its impact on diabetic parameters. Following PRISMA guidelines, a total of 11 studies were identified, both preclinical and clinical trials. Agomelatine has shown great potential as a treatment option for patients with diabetes and comorbid depression and anxiety. In addition to improving depressive and anxiety symptoms, it is also beneficial in glycemic control. A meta-analysis demonstrated a statistically significant reduction in glycated hemoglobin (HbA1C) and fasting blood glucose (FBG) levels following AGO administration over a period of 8–16 weeks. The administration of agomelatine was found to result in a significantly greater reduction in HbA1C than that observed with the selective serotonin reuptake inhibitor (SSRI) medications (namely fluoxetine, sertraline, and paroxetine) during 12–16 weeks of therapy. Furthermore, AGO has been found to be at least as effective as SSRIs in reducing depressive symptoms and more effective than SSRIs in reducing anxiety symptoms. The safety of such treatment is similar to SSRIs; no severe adverse events were reported, and the incidence of some side effects, such as insomnia and sexual dysfunction, are even less often reported. Particularly promising is also its potential action in improving some diabetic complications reported in preclinical trials. This might be through mechanisms involving the reduction in oxidative stress, anti-inflammatory effects, and potentially noradrenergic or NMDA receptor modulation. Further clinical studies on larger sample sizes, as well as elucidating its mechanisms of action, especially in the context of diabetic complications, are needed. Research should also focus on identifying the patient subpopulations most likely to benefit from agomelatine treatment. Full article
(This article belongs to the Special Issue Molecular Pharmacology of Human Metabolism Diseases)
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