Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.3
4.1
Journals
Metabolites
Special Issues
Frontiers in the Study of Metabolic Diseases Using Rodent Models
share announcement

Frontiers in the Study of Metabolic Diseases Using Rodent Models

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 12830

Special Issue Editor

Dr. Jolita Ciapaite

E-Mail Website
Guest Editor
Division Laboratories, Pharmacy and Biomedical Genetics, Section Metabolic Diagnostics, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
Interests: inborn errors of metabolism; vitamin B6 meatbolism; animal models of human disease; disease biomarker discovery; metabolomics

Special Issue Information

Dear Colleagues,

Metabolomics is an important tool in modern scientific research and clinical diagnostics. Smaller-scale targeted metabolite analyses have been used in both research and diagnostics settings for decades. In recent years, the use of untargeted, large-scale metabolite profiling, fueled by rapid developments in chromatography, mass spectrometry and nuclear magnetic resonance spectroscopy techniques, metabolite databases and data-analysis software, is gaining momentum. Metabolomics alone, or in combination with genomics (and other ‘omics’) data can  in particular be useful for understanding and later on for diagnosis of human metabolic diseases. While caused by single-gene mutations, these diseases usually are characterized by complex metabolic phenotypes, which makes quick diagnosis difficult.

This Special Issue aims to explore the contribution of metabolomics approaches to understanding the interaction between genotype, metabolism, and phenotype specifically in mouse models of human metabolic disease. The topics will include, but are not limited to, the generation and characterization of novel mouse models of human metabolic diseases, new insights in pathogenesis, interaction between disease phenotype and environmental factors, testing of treatment strategies, and preclinical biomarker discovery. Moreover, we invite manuscripts addressing the methodological challenges as well as presenting novel analytical techniques relevant to tackling the topics listed above.

Dr. Jolita Ciapaite
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. 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.

Keywords

  • Metabolic disease
  • Mouse model
  • Metabolomics
  • Mechanisms of pathogenesis
  • Phenotype and environment interactions
  • Treatment strategies
  • Preclinical biomarkers

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

12 pages, 1253 KiB  
Article
Early Effects of Metabolic Syndrome on ATP-Sensitive Potassium Channels from Rat Pancreatic Beta Cells
by Iskra Cruz-Cruz, Germán Bernate-Obando, Carlos Larqué, Rene Escalona, Rodolfo Pinto-Almazán and Myrian Velasco
Metabolites 2022, 12(4), 365; https://doi.org/10.3390/metabo12040365 - 18 Apr 2022
Cited by 3 | Viewed by 1738
Abstract
Metabolic syndrome (MS) is a cluster of metabolic signs that increases the risk of developing type 2 two diabetes mellitus and cardiovascular diseases. MS leads to pancreatic beta cell exhaustion and decreased insulin secretion through unknown mechanisms in a time-dependent manner. ATP-sensitive potassium [...] Read more.
Metabolic syndrome (MS) is a cluster of metabolic signs that increases the risk of developing type 2 two diabetes mellitus and cardiovascular diseases. MS leads to pancreatic beta cell exhaustion and decreased insulin secretion through unknown mechanisms in a time-dependent manner. ATP-sensitive potassium channels (KATP channels), common targets of anti-diabetic drugs, participate in the glucose-stimulated insulin secretion, coupling the metabolic status and electrical activity of pancreatic beta cells. We investigated the early effects of MS on the conductance, ATP and glybenclamide sensitivity of the KATP channels. We used Wistar rats fed with a high-sucrose diet (HSD) for 8 weeks as a MS model. In excised membrane patches, control and HSD channels showed similar unitary conductance and ATP sensitivity pancreatic beta cells in their KATP channels. In contrast, MS produced variability in the sensitivity to glybenclamide of KATP channels. We observed two subpopulations of pancreatic beta cells, one with similar (Gly1) and one with increased (Gly2) glybenclamide sensitivity compared to the control group. This study shows that the early effects of MS produced by consuming high-sugar beverages can affect the pharmacological properties of KATP channels to one of the drugs used for diabetes treatment. Full article
(This article belongs to the Special Issue Frontiers in the Study of Metabolic Diseases Using Rodent Models)
►▼ Show Figures

Figure 1

18 pages, 2246 KiB  
Article
High Fructose and High Fat Diet Impair Different Types of Memory through Oxidative Stress in a Sex- and Hormone-Dependent Manner
by Edwin Chávez-Gutiérrez, Claudia Erika Fuentes-Venado, Lorena Rodríguez-Páez, Christian Guerra-Araiza, Carlos Larqué, Erick Martínez-Herrera, María Esther Ocharan-Hernández, Joel Lomelí, Marco A. Loza-Mejía, Juan Rodrigo Salazar, Dulce María Meneses-Ruiz, Juan Manuel Gallardo and Rodolfo Pinto-Almazán
Metabolites 2022, 12(4), 341; https://doi.org/10.3390/metabo12040341 - 12 Apr 2022
Cited by 5 | Viewed by 2487
Abstract
Metabolic syndrome (MetS) contributes to the spread of cardiovascular diseases, diabetes mellitus type 2, and neurodegenerative diseases. Evaluation of sex- and hormone-dependent changes in body weight, blood pressure, blood lipids, oxidative stress markers, and alterations in different types of memory in Sprague–Dawley rats [...] Read more.
Metabolic syndrome (MetS) contributes to the spread of cardiovascular diseases, diabetes mellitus type 2, and neurodegenerative diseases. Evaluation of sex- and hormone-dependent changes in body weight, blood pressure, blood lipids, oxidative stress markers, and alterations in different types of memory in Sprague–Dawley rats fed with a high fat and high fructose (HFHF) diet were evaluated. After 12 weeks of feeding the male and female rats with HFHF, body weight gain, increase in blood pressure, and generation of dyslipidemia compared to the animals fed with chow diet were observed. Regarding memory, it was noted that gonadectomy reverted the effects of HFHF in the 24 h novel object recognition task and in spatial learning/memory analyzed through Morris water maze, males being more affected than females. Nevertheless, gonadectomy did not revert long-term memory impairment in the passive avoidance task induced by HFHF nor in male or female rats. On the other hand, sex-hormone–diet interaction was observed in the plasma concentration of malondialdehyde and nitric oxide. These results suggest that the changes observed in the memory and learning of MetS animals are sex- and hormone-dependent and correlate to an increase in oxidative stress. Full article
(This article belongs to the Special Issue Frontiers in the Study of Metabolic Diseases Using Rodent Models)
►▼ Show Figures

Graphical abstract

13 pages, 3100 KiB  
Article
Mitochondrial Respiration in Response to Iron Deficiency Anemia: Comparison of Peripheral Blood Mononuclear Cells and Liver
by Christine Fischer, Lara Valente de Souza, Timea Komlódi, Luiz F. Garcia-Souza, Chiara Volani, Piotr Tymoszuk, Egon Demetz, Markus Seifert, Kristina Auer, Richard Hilbe, Natascha Brigo, Verena Petzer, Malte Asshoff, Erich Gnaiger and Günter Weiss
Metabolites 2022, 12(3), 270; https://doi.org/10.3390/metabo12030270 - 21 Mar 2022
Cited by 4 | Viewed by 2754
Abstract
Iron is an essential component for metabolic processes, including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity, and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA), which affects approximately 1.5 billion [...] Read more.
Iron is an essential component for metabolic processes, including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity, and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA), which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) and the liver. Furthermore, we evaluated whether the mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to the controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and the liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue. Full article
(This article belongs to the Special Issue Frontiers in the Study of Metabolic Diseases Using Rodent Models)
►▼ Show Figures

Graphical abstract

17 pages, 12906 KiB  
Article
Changes in Plasma Lipid Levels Following Cortical Spreading Depolarization in a Transgenic Mouse Model of Familial Hemiplegic Migraine
by Inge C. M. Loonen, Isabelle Kohler, Mohan Ghorasaini, Martin Giera, Arn M. J. M. van den Maagdenberg, Oleg A. Mayboroda and Else A. Tolner
Metabolites 2022, 12(3), 220; https://doi.org/10.3390/metabo12030220 - 1 Mar 2022
Cited by 1 | Viewed by 2582
Abstract
Metabolite levels in peripheral body fluids can correlate with attack features in migraine patients, which underscores the potential of plasma metabolites as possible disease biomarkers. Migraine headache can be preceded by an aura that is caused by cortical spreading depolarization (CSD), a transient [...] Read more.
Metabolite levels in peripheral body fluids can correlate with attack features in migraine patients, which underscores the potential of plasma metabolites as possible disease biomarkers. Migraine headache can be preceded by an aura that is caused by cortical spreading depolarization (CSD), a transient wave of neuroglial depolarization. We previously identified plasma amino acid changes after CSD in familial hemiplegic migraine type 1 (FHM1) mutant mice that exhibit increased neuronal excitability and various migraine-related features. Here, we aimed to uncover lipid metabolic pathways affected by CSD, guided by findings on the involvement of lipids in hemiplegic migraine pathophysiology. Using targeted lipidomic analysis, we studied plasma lipid metabolite levels at different time points after CSD in wild-type and FHM1 mutant mice. Following CSD, the most prominent plasma lipid change concerned a transient increase in PGD2, which lasted longer in mutant mice. In wild-type mice only, levels of anti-inflammatory lipid mediators DPAn-3, EPA, ALA, and DHA were elevated 24 h following CSD compared to Sham-treated animals. Given the role of PGs and neuroinflammation in migraine pathophysiology, our findings underscore the potential of monitoring peripheral changes in lipids to gain insight in central brain mechanisms. Full article
(This article belongs to the Special Issue Frontiers in the Study of Metabolic Diseases Using Rodent Models)
►▼ Show Figures

Graphical abstract

13 pages, 1271 KiB  
Article
Hepatic Response of Magnesium-Restricted Wild Type Mice
by Vera H. Fengler, Tanja Macheiner, Walter Goessler, Maria Ratzer, Johannes Haybaeck and Karine Sargsyan
Metabolites 2021, 11(11), 762; https://doi.org/10.3390/metabo11110762 - 6 Nov 2021
Cited by 5 | Viewed by 1975
Abstract
Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice [...] Read more.
Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the hepatic inflammatory response was quantified by determining hepatic IL-6, TNFα, and MCP-1. Magnesium-restriction resulted in at least a 2-fold significant reduction of serum magnesium levels compared to the high-fat-diet fed and control mice, whereas the hepatic magnesium content was decreased due to high-fat-diet feeding. No changes in metabolic markers in magnesium-restricted mice were observed, while the cholesterol content was elevated in high-fat-diet fed mice. Magnesium-restricted mice additionally featured inflammation and enlarged hepatocytes in liver histology. Furthermore, magnesium-restricted and high-fat-diet fed mice exhibited elevated hepatic TNFα levels compared to control mice. Accordingly, our data suggest that magnesium is involved in hepatic inflammatory processes and hepatocyte enlargement, key histological features of human NAFLD, and may therefore contribute to development and progression of the disease. Full article
(This article belongs to the Special Issue Frontiers in the Study of Metabolic Diseases Using Rodent Models)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop