Metabolites

Journal Browser

► Journal Browser

Cellular Metabolism Related to Metabolic Syndrome

Special Issue Editors
Special Issue Information
Published Papers

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 3852

Share This Special Issue

Special Issue Editors

Prof. Dr. Kuo-Chin Huang

E-Mail Website
Guest Editor

Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
Interests: obesity; management of obesity; obesity-related biomarkers
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Chichang Huang

E-Mail Website
Guest Editor

Graduate Institute of Sports Science, National Taiwan Sport University, Taoyuan City 333325, Taiwan
Interests: functional ingredients; sports nutrition; herbal medicine

Special Issue Information

Dear Colleagues,

Cell metabolism can be divided into anabolism and catabolism. It is a series of chemical reactions that occur in the organism in order to maintain life and are organized into metabolic pathways that enable the organism to grow and reproduce, maintain its structure, and respond to environmental changes. Therefore, most of the key cellular decision-making processes in cells involve, or are closely related to, metabolic changes. Conversely, disturbances in the abundance or quantity of metabolites can adversely alter cellular processes and lead to altered functional states at an organism level that may subsequently lead to disease. Metabolic syndrome refers to a cluster of related conditions where pathophysiological defects in energy utilization and/or conversion occur. Examples include cardiovascular disease, obesity, altered blood lipids, and abnormal blood sugar metabolism. In this Special Issue, we invite original research and review articles that focus on the efficiency and mechanisms involved in cell metabolism related to anabolic enzymes, the influence or diet, sugar metabolism, and related aspects that pertain to metabolic syndrome.

Prof. Dr. Kuo-Chin Huang
Prof. Dr. Chichang Huang
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. Metabolites 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 2700 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.

Published Papers (2 papers)

Download All Papers

Research

Jump to: Other

15 pages, 3939 KiB

Open AccessArticle

Intravenous Arginine Administration Attenuates the Inflammatory Response and Improves Metabolic Profiles in Diet-Induced Obese Mice after Sleeve Gastrectomy

by Ya-Ling Chen, Ming-Tsan Lin, Wan-Hsuan Wang, Sung-Ling Yeh and Chiu-Li Yeh

Metabolites 2022, 12(2), 153; https://doi.org/10.3390/metabo12020153 - 7 Feb 2022

Cited by 3 | Viewed by 1619

Abstract

Sleeve gastrectomy (SG) is a bariatric surgery that can effectively reduce weight and improve obesity-associated comorbidities. However, surgical stress intensifies inflammation and imbalanced metabolic profiles. Arginine (Arg) is a nutrient with immunomodulatory and anti-inflammatory properties. This study evaluated the short-term effects of Arg administration on adipocyte inflammation and metabolic alterations in obese mice after SG. Mice were assigned to normal and high-fat diet (HFD) groups. After 16 weeks, the HFD group were divided to sham (SH), SG with saline (SS), or Arg (SA) groups. SS and SA groups were postoperatively injected with saline or Arg via the tail vein and sacrificed at day 1 or 3 after the SG, respectively. Results showed that obesity caused elevated plasma glucose and leptin levels. The SG operation enhanced the expression of inflammatory cytokines and macrophage infiltration in adipose tissues, whereas hepatocyte gene expressions associated with lipid β-oxidation were downregulated. Arg treatment reversed the expressions of β-oxidation-associated genes and reduced lipid peroxide production in the liver. Additionally, adipose tissue expressions of inflammatory chemokines were reduced, while the M2 macrophage marker increased after surgery. The findings suggest that postoperative Arg administration elicited more balanced hepatic lipid metabolism, polarized macrophages toward the anti-inflammatory type, and attenuated adipocyte inflammation shortly after SG. Full article

(This article belongs to the Special Issue Cellular Metabolism Related to Metabolic Syndrome)

► Show Figures

Figure 1

Other

Jump to: Research

7 pages, 860 KiB

Open AccessBrief Report

Intracellular Toxic Advanced Glycation End-Products May Induce Cell Death and Suppress Cardiac Fibroblasts

by Takanobu Takata, Akiko Sakasai-Sakai and Masayoshi Takeuchi

Metabolites 2022, 12(7), 615; https://doi.org/10.3390/metabo12070615 - 1 Jul 2022

Cited by 7 | Viewed by 1568

Abstract

Cardiovascular disease (CVD) is a lifestyle-related disease (LSRD) induced by the dysfunction and cell death of cardiomyocytes. Cardiac fibroblasts are activated and differentiate in response to specific signals, such as transforming growth factor-β released from injured cardiomyocytes, and are crucial for the protection of cardiomyocytes, cardiac tissue repair, and remodeling. In contrast, cardiac fibroblasts have been shown to induce injury or death of cardiomyocytes and are implicated in the pathogenesis of diseases such as cardiac hypertrophy. We designated glyceraldehyde-derived advanced glycation end-products (AGEs) as toxic AGEs (TAGE) due to their cytotoxicity and association with LSRD. Intracellular TAGE in cardiomyocytes decreased their beating rate and induced cell death in the absence of myocardial ischemia. The TAGE levels in blood were elevated in patients with CVD and were associated with myocardial ischemia along with increased risk of atherosclerosis in vascular endothelial cells in vitro. The relationships between the dysfunction or cell death of cardiac fibroblasts and intracellular and extracellular TAGE, which are secreted from certain organs, remain unclear. We examined the cytotoxicity of intracellular TAGE by a slot blot analysis, and TAGE-modified bovine serum albumin (TAGE-BSA), a model of extracellular TAGE, in normal human cardiac fibroblasts (HCF). Intracellular TAGE induced cell death in normal HCF, whereas TAGE-BSA did not, even at aberrantly high non-physiological levels. Therefore, only intracellular TAGE induced cell death in HCF under physiological conditions, possibly inhibiting the role of HCF. Full article

(This article belongs to the Special Issue Cellular Metabolism Related to Metabolic Syndrome)

► Show Figures