Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications

Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

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

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 5275

Share This Special Issue

Special Issue Editor

Dr. Myunggon Ko

E-Mail Website
Guest Editor

Department of Biological Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea
Interests: DNA methylation; TET proteins; hematopoietic stem cells; hematopoiesis; leukemia; cancer epigenetics; cancer therapy; drug screen; metabolic diseases; obesity; diabetes; biosensor; signaling and gene expression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolism, the cornerstone of life, is finely orchestrated by the complex interplay among cells within specialized tissues, notably adipocytes, muscle cells, and hepatocytes. Adipocytes govern systemic energy and glucose homeostasis, thermogenesis, and hormone secretion. Muscle cells, with their high energy demands, also play a central role in glucose uptake and utilization. Dysfunction within these cells disrupts the metabolic balance, contributing to various complications, including insulin resistance, obesity, diabetes, and cardiovascular diseases. Additionally, hepatocytes, the metabolic powerhouses, also dictate glucose and lipid metabolism and detoxification, and they are the central players in diabetes, fatty liver disease, hepatic inflammation and fibrosis, and liver cancers. This Special Issue aims to explore the intricate molecular events and mechanisms that underlie both normal and aberrant cellular metabolism, along with the associated metabolic disorders.

We invite submissions of original research articles, reviews, and clinical studies that address, but are not limited to, the following areas:

Molecular insights into adipocyte differentiation and function;
Adipose tissue inflammation and metabolic dysfunction;
Role of adipokines in metabolism;
Adipose tissue remodeling in health and disease;
Hepatic glucose and lipid metabolism;
Crosstalk among liver, muscle, and adipose tissues in metabolic regulation;
Genetic and epigenetic regulation of metabolism;
Obesity and diabetes: mechanisms, complications, and therapeutic interventions;
Steatosis, hepatitis, and cirrhosis: underlying mechanisms and therapeutic targets;
Liver cancers: pathology and therapeutic strategies;
Innovative therapeutic approaches to treat metabolic diseases.

We look forward to receiving your contributions.

Dr. Myunggon Ko
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

cell metabolism
adipocytes
muscle cells
hepatocytes
insulin resistance
inflammation
obesity
diabetes
hepatic disorders
cardiovascular diseases
cancers

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

14 pages, 2258 KiB

Open AccessArticle

Effects of Fentanyl-Laced Cocaine on Circulating Ghrelin, Insulin, and Glucose Levels in Rats

by Huimei Wei, Elise C. Maul, Annet Kyomuhangi, Shawn Park, Maddilynn L. Mutchler, Chang-Guo Zhan and Fang Zheng

Int. J. Mol. Sci. 2025, 26(5), 2341; https://doi.org/10.3390/ijms26052341 - 6 Mar 2025

Viewed by 104

Abstract

Opioid mixed with cocaine has been increasingly implicated in overdose deaths, including both intentional co-use of opioid and cocaine and fentanyl-adulterated drug supply. As ghrelin plays an important role in drug reward and can also influence insulin, this study aimed to assess responses of the circulating ghrelin, insulin, and glucose levels to the combined use of fentanyl and cocaine (a polydrug) in rats by performing combined animal behavioral experiments and biochemical analysis. The experimental data consistently revealed that the fentanyl and cocaine co-use can significantly elevate both the acyl-ghrelin and desacyl-ghrelin levels and significantly decrease the insulin level without significant effects on the glucose level. These findings suggest that, like cocaine itself, the fentanyl–cocaine polydrug can self-promote its rewarding effects via elevating the ghrelin level, and that the ghrelin system might serve as a potential pharmacological target for treatment of substance use disorders caused by polysubstance use involving fentanyl and cocaine. Additionally, based on the insulin data obtained in this study, the insulin level was always downregulated significantly and considerably, implying that the fentanyl and cocaine polydrug might have a stronger cardiovascular toxicity to the patients with insulin resistance and diabetes. Further studies are required to examine this possibility. Full article

(This article belongs to the Special Issue Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications)

► Show Figures

Figure 1

13 pages, 2220 KiB

Open AccessArticle

Oligonol^®, an Oligomerized Polyphenol from Litchi chinensis, Enhances Branched-Chain Amino Acid Transportation and Catabolism to Alleviate Sarcopenia

by Yun-Ching Chang, Yu-Chi Chen, Yin-Ching Chan, Cheng Liu and Sue-Joan Chang

Int. J. Mol. Sci. 2024, 25(21), 11549; https://doi.org/10.3390/ijms252111549 - 27 Oct 2024

Viewed by 1376

Abstract

Branched-chain amino acids (BCAAs) are essential for muscle protein synthesis and are widely acknowledged for mitigating sarcopenia. Oligonol^® (Olg), a low-molecular-weight polyphenol from Litchi chinensis, has also been found to attenuate sarcopenia by improving mitochondrial quality and positive protein turnover. This study aims to investigate the effect of Olg on BCAA-stimulated protein synthesis in sarcopenia. In sarcopenic C57BL/6 mice and senescence-accelerated mouse-prone 8 (SAMP8) mice, BCAAs were significantly decreased in skeletal muscle but increased in blood serum. Furthermore, the expressions of membrane L-type amino acid transporter 1 (LAT1) and branched-chain amino acid transaminase 2 (BCAT2) in skeletal muscle were lower in aged mice than in young mice. The administration of Olg for 8 weeks significantly increased the expressions of membrane LAT1 and BCAT2 in the skeletal muscle when compared with non-treated SAMP8 mice. We further found that BCAA deprivation via LAT1-siRNA in C2C12 myotubes inhibited the signaling of protein synthesis and facilitated ubiquitination degradation of BCAT2. In C2C12 cells mimicking sarcopenia, Olg combined with BCAA supplementation enhanced mTOR/p70S6K activity more than BCAA alone. However, blocked LAT1 by JPH203 reversed the synergistic effect of the combination of Olg and BCAAs. Taken together, changes in LAT1 and BCAT2 during aging profoundly alter BCAA availability and nutrient signaling in aged mice. Olg increases BCAA-stimulated protein synthesis via modulating BCAA transportation and BCAA catabolism. Combining Olg and BCAAs may be a useful nutritional strategy for alleviating sarcopenia. Full article

(This article belongs to the Special Issue Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications)

► Show Figures

Figure 1

Review

Jump to: Research

23 pages, 2243 KiB

Open AccessReview

Combining Photodynamic Therapy and Targeted Drug Delivery Systems: Enhancing Mitochondrial Toxicity for Improved Cancer Outcomes

by J. P. Jose Merlin, Anine Crous and Heidi Abrahamse

Int. J. Mol. Sci. 2024, 25(19), 10796; https://doi.org/10.3390/ijms251910796 - 8 Oct 2024

Cited by 1 | Viewed by 2395

Abstract

Cancer treatment continues to be a substantial problem due to tumor complexities and persistence, demanding novel therapeutic techniques. This review investigates the synergistic potential of combining photodynamic therapy (PDT) and tailored medication delivery technologies to increase mitochondrial toxicity and improve cancer outcomes. PDT induces selective cellular damage and death by activating photosensitizers (PS) with certain wavelengths of light. However, PDT’s efficacy can be hampered by issues such as poor light penetration and a lack of selectivity. To overcome these challenges, targeted drug delivery systems have emerged as a promising technique for precisely delivering therapeutic medicines to tumor cells while avoiding off-target effects. We investigate how these technologies can improve mitochondrial targeting and damage, which is critical for causing cancer cell death. The combination method seeks to capitalize on the advantages of both modalities: selective PDT activation and specific targeted drug delivery. We review current preclinical and clinical evidence supporting the efficacy of this combination therapy, focusing on case studies and experimental models. This review also addresses issues such as safety, distribution efficiency, resistance mechanisms, and costs. The prospects of further research include advances in photodynamic agents and medication delivery technology, with a focus on personalized treatment. In conclusion, combining PDT with targeted drug delivery systems provides a promising frontier in cancer therapy, with the ability to overcome current treatment limits and open the way for more effective, personalized cancer treatments. Full article

(This article belongs to the Special Issue Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications)

► Show Figures

Journal Menu

Journal Browser

Cell Metabolism: Its Physiology, Dysfunction, and Related Metabolic Complications

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (3 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI