ijms-logo

Journal Browser

Journal Browser

Molecular Research on Carbohydrate Metabolism

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 (15 February 2023) | Viewed by 10521

Special Issue Editors


E-Mail Website
Guest Editor
1. Department of Biological Sciences, College of Science, Sungkyunkwan University, Seoburo 2066, Suwon 16419, Republic of Korea
2. Samsung Advanced Institute of Health Science and Technology (SAIHST), Sungkyunkwan University, Seoul 06351, Republic of Korea
Interests: glycobiology; sialobiology; sialyltransferase; N-glycan; O-glycan; glycolipid; sphingolipid; glycoprotein; surface sugar; ganglioside; sialic acid; Sialyl Le antigen; lectin; galectin; Siglec; ER-Golgi glycosylation; sugar–receptor interaction; innate immune; xenotransplantation; cell–cell interaction
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biomedicine Imaging and Radiological Science, National Yang Ming Chiao Tung University, Taipei 112, Taiwan
Interests: cancer metabolism; radiobiology; biomolecular imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the 1920s, the Warburg group discovered that tumors acquire large amounts of glucose rather than normal cells. This glucose is anaerobically metabolized to lactate even in normoxic conditions, a phenomenon known as aerobic glycolysis. Since tumor cells are viable during respiration, elimination of glucose and oxygen has been tried out in order to kill tumor cells. Respiration in tumors is evolutionarily adapted to both of aerobic and anaerobic glycolysis. The Warburg effect is widely recognized in the field of cancer study. Developing a more in-depth understanding of glycolytic adaptation in tumor cells will open new vistas to achieve their regression, if the evidence that has been gathered so far is anything to go by.

In cell, tissue, organ, and individual sides, monosaccharide (glucose) is considered the basic unit and main nutrient resource for maintaining human physiological functions and metabolism. Carbohydrate metabolic reprogramming and its related enzyme activity abnormalities are regarded as the key factors related to chronic diseases, inflammation, and even carcinogenesis. These changes include glycolysis, tricarboxylic acid (TCA) cycle, mitochondrial function, pentose phosphate pathway (PPP), and gluconeogenesis. Our goal is to show the enzyme activity, transporters, metabolites, and gene expression among them and indicate their prognostic value, probes, modulators, and therapeutic targets.

We encourage the publication of original research articles and comments that cover all aspects of glycolytic enzymes. Contributions to this Special Issue will provide new insights into the mechanisms and functions of carbohydrate metabolism, deepen our understanding of their biological role in health and disease, and reveal novel aspects of therapeutic opportunities.

Prof. Dr. Cheorl-Ho Kim
Dr. Yu-Chan Chang
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.

Keywords

  • glycolysis/TCA cycle/pentose phosphate pathway/gluconeogenesis
  • metabolic reprogramming
  • regulation
  • signaling transduction
  • metabolites
  • biosensors

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

24 pages, 3008 KiB  
Article
Lack of TRPV1 Channel Modulates Mouse Gene Expression and Liver Proteome with Glucose Metabolism Changes
by José Thalles Lacerda, Patrícia R. L. Gomes, Giovanna Zanetti, Nathana Mezzalira, Otoniel G. Lima, Leonardo V. M. de Assis, Ali Guler, Ana Maria Castrucci and Maria Nathália Moraes
Int. J. Mol. Sci. 2022, 23(13), 7014; https://doi.org/10.3390/ijms23137014 - 24 Jun 2022
Cited by 8 | Viewed by 2742
Abstract
To investigate the role of the transient receptor potential channel vanilloid type 1 (TRPV1) in hepatic glucose metabolism, we analyzed genes related to the clock system and glucose/lipid metabolism and performed glycogen measurements at ZT8 and ZT20 in the liver of C57Bl/6J (WT) [...] Read more.
To investigate the role of the transient receptor potential channel vanilloid type 1 (TRPV1) in hepatic glucose metabolism, we analyzed genes related to the clock system and glucose/lipid metabolism and performed glycogen measurements at ZT8 and ZT20 in the liver of C57Bl/6J (WT) and Trpv1 KO mice. To identify molecular clues associated with metabolic changes, we performed proteomics analysis at ZT8. Liver from Trpv1 KO mice exhibited reduced Per1 expression and increased Pparα, Pparγ, Glut2, G6pc1 (G6pase), Pck1 (Pepck), Akt, and Gsk3b expression at ZT8. Liver from Trpv1 KO mice also showed reduced glycogen storage at ZT8 but not at ZT20 and significant proteomics changes consistent with enhanced glycogenolysis, as well as increased gluconeogenesis and inflammatory features. The network propagation approach evidenced that the TRPV1 channel is an intrinsic component of the glucagon signaling pathway, and its loss seems to be associated with increased gluconeogenesis through PKA signaling. In this sense, the differentially identified kinases and phosphatases in WT and Trpv1 KO liver proteomes show that the PP2A phosphatase complex and PKA may be major players in glycogenolysis in Trpv1 KO mice. Full article
(This article belongs to the Special Issue Molecular Research on Carbohydrate Metabolism)
Show Figures

Graphical abstract

Review

Jump to: Research

23 pages, 992 KiB  
Review
Application of Metabolic Reprogramming to Cancer Imaging and Diagnosis
by Yi-Fang Yang, Chien-Hsiu Li, Huei-Yu Cai, Bo-Syuan Lin, Cheorl-Ho Kim and Yu-Chan Chang
Int. J. Mol. Sci. 2022, 23(24), 15831; https://doi.org/10.3390/ijms232415831 - 13 Dec 2022
Cited by 1 | Viewed by 1665
Abstract
Cellular metabolism governs the signaling that supports physiological mechanisms and homeostasis in an individual, including neuronal transmission, wound healing, and circadian clock manipulation. Various factors have been linked to abnormal metabolic reprogramming, including gene mutations, epigenetic modifications, altered protein epitopes, and their involvement [...] Read more.
Cellular metabolism governs the signaling that supports physiological mechanisms and homeostasis in an individual, including neuronal transmission, wound healing, and circadian clock manipulation. Various factors have been linked to abnormal metabolic reprogramming, including gene mutations, epigenetic modifications, altered protein epitopes, and their involvement in the development of disease, including cancer. The presence of multiple distinct hallmarks and the resulting cellular reprogramming process have gradually revealed that these metabolism-related molecules may be able to be used to track or prevent the progression of cancer. Consequently, translational medicines have been developed using metabolic substrates, precursors, and other products depending on their biochemical mechanism of action. It is important to note that these metabolic analogs can also be used for imaging and therapeutic purposes in addition to competing for metabolic functions. In particular, due to their isotopic labeling, these compounds may also be used to localize and visualize tumor cells after uptake. In this review, the current development status, applicability, and limitations of compounds targeting metabolic reprogramming are described, as well as the imaging platforms that are most suitable for each compound and the types of cancer to which they are most appropriate. Full article
(This article belongs to the Special Issue Molecular Research on Carbohydrate Metabolism)
Show Figures

Figure 1

21 pages, 905 KiB  
Review
Revisited Metabolic Control and Reprogramming Cancers by Means of the Warburg Effect in Tumor Cells
by Abekura Fukushi, Hee-Do Kim, Yu-Chan Chang and Cheorl-Ho Kim
Int. J. Mol. Sci. 2022, 23(17), 10037; https://doi.org/10.3390/ijms231710037 - 2 Sep 2022
Cited by 37 | Viewed by 5247
Abstract
Aerobic glycolysis is an emerging hallmark of many human cancers, as cancer cells are defined as a “metabolically abnormal system”. Carbohydrates are metabolically reprogrammed by its metabolizing and catabolizing enzymes in such abnormal cancer cells. Normal cells acquire their energy from oxidative phosphorylation, [...] Read more.
Aerobic glycolysis is an emerging hallmark of many human cancers, as cancer cells are defined as a “metabolically abnormal system”. Carbohydrates are metabolically reprogrammed by its metabolizing and catabolizing enzymes in such abnormal cancer cells. Normal cells acquire their energy from oxidative phosphorylation, while cancer cells acquire their energy from oxidative glycolysis, known as the “Warburg effect”. Energy–metabolic differences are easily found in the growth, invasion, immune escape and anti-tumor drug resistance of cancer cells. The glycolysis pathway is carried out in multiple enzymatic steps and yields two pyruvate molecules from one glucose (Glc) molecule by orchestral reaction of enzymes. Uncontrolled glycolysis or abnormally activated glycolysis is easily observed in the metabolism of cancer cells with enhanced levels of glycolytic proteins and enzymatic activities. In the “Warburg effect”, tumor cells utilize energy supplied from lactic acid-based fermentative glycolysis operated by glycolysis-specific enzymes of hexokinase (HK), keto-HK-A, Glc-6-phosphate isomerase, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase, phosphofructokinase (PFK), phosphor-Glc isomerase (PGI), fructose-bisphosphate aldolase, phosphoglycerate (PG) kinase (PGK)1, triose phosphate isomerase, PG mutase (PGAM), glyceraldehyde-3-phosphate dehydrogenase, enolase, pyruvate kinase isozyme type M2 (PKM2), pyruvate dehydrogenase (PDH), PDH kinase and lactate dehydrogenase. They are related to glycolytic flux. The key enzymes involved in glycolysis are directly linked to oncogenesis and drug resistance. Among the metabolic enzymes, PKM2, PGK1, HK, keto-HK-A and nucleoside diphosphate kinase also have protein kinase activities. Because glycolysis-generated energy is not enough, the cancer cell-favored glycolysis to produce low ATP level seems to be non-efficient for cancer growth and self-protection. Thus, the Warburg effect is still an attractive phenomenon to understand the metabolic glycolysis favored in cancer. If the basic properties of the Warburg effect, including genetic mutations and signaling shifts are considered, anti-cancer therapeutic targets can be raised. Specific therapeutics targeting metabolic enzymes in aerobic glycolysis and hypoxic microenvironments have been developed to kill tumor cells. The present review deals with the tumor-specific Warburg effect with the revisited viewpoint of recent progress. Full article
(This article belongs to the Special Issue Molecular Research on Carbohydrate Metabolism)
Show Figures

Graphical abstract

Back to TopTop