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Biomedicines
Special Issues
Metabolic Diseases Regulators
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Metabolic Diseases Regulators

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1498

Special Issue Editor

Dr. Mariana Georgeta Roșca

E-Mail Website
Guest Editor
Department of Foundational Sciences, Central Michigan University College of Medicine, Mount Pleasant, MI 48858, USA
Interests: mitochondria; metabolism; bioenergetics; metabolic syndrome; mitochondrial defects

Special Issue Information

Dear Colleagues,

Metabolic syndrome is a group of metabolic abnormalities centered around excessive visceral adiposity that involves diseases in target organs, mainly cardiovascular system, skeletal muscle, pancreas and liver. Diseases associated with metabolic syndrome are associated with a high level of morbidity and mortality. Treating organ diseases that are induced by metabolic syndrome is cumbersome. Therefore, identifying common pathogenic mechanisms and specific factors is the focus of multidisciplinary approaches, the aim of which is to translate this knowledge into prevention and therapy. This Special Issue is focused on unfolding the role of novel regulators that are involved in the development of the metabolic syndrome and related organ diseases. The scope is to reveal potential therapeutic targets that are common for metabolic diseases.

Dr. Mariana Georgeta Roșca
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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 syndrome
  • obesity
  • visceral adiposity
  • insulin resistance
  • type 2 diabetes
  • diabetic cardiomyopathy
  • non-alcoholic fatty liver disease

Published Papers (2 papers)

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Research

15 pages, 8102 KiB  
Article
Hydrogen-Rich Water (HRW) Reduces Fatty Acid-Induced Lipid Accumulation and Oxidative Stress Damage through Activating AMP-Activated Protein Kinase in HepG2 Cells
by Sing-Hua Tsou, Sheng-Chieh Lin, Wei-Jen Chen, Hui-Chih Hung, Chun-Cheng Liao, Edy Kornelius, Chien-Ning Huang, Chih-Li Lin and Yi-Sun Yang
Biomedicines 2024, 12(7), 1444; https://doi.org/10.3390/biomedicines12071444 - 28 Jun 2024
Viewed by 297
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by excessive fat accumulation in the liver. Intracellular oxidative stress induced by lipid accumulation leads to various hepatocellular injuries including fibrosis. However, no effective method for mitigating MASLD without substantial side effects currently exists. Molecular [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by excessive fat accumulation in the liver. Intracellular oxidative stress induced by lipid accumulation leads to various hepatocellular injuries including fibrosis. However, no effective method for mitigating MASLD without substantial side effects currently exists. Molecular hydrogen (H2) has garnered attention due to its efficiency in neutralizing harmful reactive oxygen species (ROS) and its ability to penetrate cell membranes. Some clinical evidence suggests that H2 may alleviate fatty liver disease, but the precise molecular mechanisms, particularly the regulation of lipid droplet (LD) metabolism, remain unclear. This study utilized an in vitro model of hepatocyte lipid accumulation induced by free fatty acids (FFAs) to replicate MASLD in HepG2 cells. The results demonstrated a significant increase in LD accumulation due to elevated FFA levels. However, the addition of hydrogen-rich water (HRW) effectively reduced LD accumulation. HRW decreased the diameter of LDs and reduced lipid peroxidation and FFA-induced oxidative stress by activating the AMPK/Nrf2/HO-1 pathway. Overall, our findings suggest that HRW has potential as an adjunctive supplement in managing fatty liver disease by reducing LD accumulation and enhancing antioxidant pathways, presenting a novel strategy for impeding MASLD progression. Full article
(This article belongs to the Special Issue Metabolic Diseases Regulators)
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14 pages, 3851 KiB  
Article
Pathogenic Homocystinuria-Associated T236N Mutation Dramatically Alters the Biochemical Properties of Cystathionine Beta-Synthase Protein
by Duaa W. Al-Sadeq, Angelos Thanassoulas, Maria Theodoridou, Gheyath K. Nasrallah and Michail Nomikos
Biomedicines 2024, 12(5), 929; https://doi.org/10.3390/biomedicines12050929 - 23 Apr 2024
Viewed by 753
Abstract
Background: Cystathione beta-synthase (CBS) T236N is a novel mutation associated with pyridoxine non-responsiveness, which presents a significant difficulty in the medical treatment of homocystinuria. Reported severe phenotypes in homocystinuria patients highlight the urgent requirement to comprehend the molecular mechanisms underlying mutation pathogenicity for [...] Read more.
Background: Cystathione beta-synthase (CBS) T236N is a novel mutation associated with pyridoxine non-responsiveness, which presents a significant difficulty in the medical treatment of homocystinuria. Reported severe phenotypes in homocystinuria patients highlight the urgent requirement to comprehend the molecular mechanisms underlying mutation pathogenicity for the advancement of the disease. Methodology: In this study, we used a multidisciplinary approach to investigate the molecular properties of bacterially expressed and purified recombinant CBST236N protein, which we directly compared to those of the wild-type (CBSWT) protein. Results: Our data revealed a profound impact of the p.T236N mutation on CBS enzymatic activity, with a dramatic reduction of ~96% compared to the CBSWT protein. Circular dichroism (CD) experiments indicated that the p.T236N mutation did not significantly alter the secondary structure of the protein. However, CD spectra unveiled distinct differences in the thermal stability of CBSWT and CBST236N mutant protein species. In addition, chemical denaturation experiments further highlighted that the CBSWT protein exhibited greater thermodynamic stability than the CBST236N mutant, suggesting a destabilizing effect of this mutation. Conclusions: Our findings provide an explanation of the pathogenicity of the p.T236N mutation, shedding light on its role in severe homocystinuria phenotypes. This study contributes to a deeper understanding of CBS deficiency and may improve the development of targeted therapeutic strategies for affected individuals. Full article
(This article belongs to the Special Issue Metabolic Diseases Regulators)
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