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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: 20 February 2025 | Viewed by 1867

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 (2 papers)

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Research

27 pages, 6717 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
Viewed by 317
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 1007
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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