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Advances in Murine Models for Metabolic Diseases: Insights into Diabetes,...
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Advances in Murine Models for Metabolic Diseases: Insights into Diabetes, Obesity, and Cardiovascular Conditions

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

Deadline for manuscript submissions: 31 August 2026 | Viewed by 6644

Special Issue Editor

Prof. Dr. Samuel Treviño

E-Mail Website
Guest Editor
Laboratory of Metabolomic and Chronic Degenerative Diseases, Physiology Institute, Meritorious Autonomous University of Puebla, Puebla C.P. 72560, Mexico
Interests: metabolic diseases; chronic degenerative diseases; endocrinology; inflammation; oxidative stress; biochemistry; molecular biology

Special Issue Information

Dear Colleagues,

Advances in murine models are crucial for understanding the complex interplay of metabolic diseases like diabetes, obesity, and cardiovascular conditions. This Special Issue of Metabolites focuses on cutting-edge research utilizing these models to dissect disease mechanisms and identify potential therapeutic targets.

Focus: This Special Issue emphasizes innovative approaches in the murine modeling of metabolic diseases. This includes genetically modified mice (e.g., knockouts, knock-ins, and transgenics), diet-induced models (e.g., high-fat diet and high-fructose diet), and combined approaches that mimic the multifaceted nature of human diseases. We also encourage submissions exploring the impact of gut microbiota, inflammation, and other contributing factors on metabolic dysfunction in these models.

Scope: This Special Issue covers a broad spectrum of research areas, including the following:

  • Mechanistic studies investigating the molecular pathways involved in disease development and progression.
  • Preclinical testing of novel therapeutic interventions, including pharmacological agents, dietary interventions, and gene therapies.
  • Studies exploring the link between metabolic disorders and related complications, such as cardiovascular disease, neuropathy, and nephropathy.
  • Development and validation of new techniques for assessing metabolic phenotypes in mice, including metabolomics, imaging, and physiological measurements.

Purpose: This Special Issue aims at providing a comprehensive overview of the current state of the art in murine models of metabolic diseases. It serves as a valuable resource for researchers in the field, facilitating the exchange of knowledge and fostering collaborations. By highlighting recent advances and identifying knowledge gaps, this Special Issue will guide future research and accelerate the development of effective strategies for preventing and treating human metabolic disorders.

Prof. Dr. Samuel Treviño
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 250 words) can be sent to the Editorial Office for assessment.

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

  • murine models
  • metabolic diseases
  • molecular mechanisms
  • biochemical pathways
  • pharmacological strategies
  • interactome
  • comorbidities
  • metabolic phenotypes
  • novel techniques

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

Published Papers (4 papers)

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Research

20 pages, 2383 KB  
Article
Synergistic Effects of Obesity and Hyperglycemia on Hippocampal Neurodegenerative Decline Disrupt the Neural Circuitry Regulating Motivation in Zucker Diabetic Fatty Rats
by Martha Patricia Islas-Islas, Aleida Monserrat Coss-Orozco, Diana Moroni-González, Erick Flores-Cholula, José Everardo Avelino-Cruz, Julio Cesar Morales-Medina, Alfonso Diaz, Fabián Galindo-Ramírez, Samuel Treviño and Rubén Antonio Vázquez-Roque
Metabolites 2026, 16(2), 107; https://doi.org/10.3390/metabo16020107 - 3 Feb 2026
Viewed by 950
Abstract
Background/Objectives: Type 2 diabetes (T2D) and obesity are chronic metabolic disorders associated with cognitive impairment and neuronal damage. The hippocampus, a region sensitive to nutrient excess, is critical for integrating sensory and metabolic signals. This study aimed to determine the early onset [...] Read more.
Background/Objectives: Type 2 diabetes (T2D) and obesity are chronic metabolic disorders associated with cognitive impairment and neuronal damage. The hippocampus, a region sensitive to nutrient excess, is critical for integrating sensory and metabolic signals. This study aimed to determine the early onset of cognitive and motor deficits induced by obesity and/or hyperglycemia and to characterize associated hippocampal alterations in Zucker Diabetic Fatty (ZDF) rats. Methods: Male ZDF rats (13 weeks old) were categorized into three groups: lean control, obese normoglycemic (ZDF-NG), and obese hyperglycemic (ZDF-HG). Assessments included zoometric parameters (weight and adiposity), biochemical assays (glucose tolerance, insulin response, and lipid profile), and behavioral tests (Open Field and Novel Object Recognition). Hippocampal health was evaluated through stereological neuronal density analysis and redox balance markers. Results: Both obese groups exhibited significant visceral adiposity and hyperlipidemia. The ZDF-HG group was further characterized by glucose intolerance, hepatic insulin resistance, and reduced β-cell function. Behavioral results showed that while obesity decreased motor activity, hyperglycemia significantly exacerbated the loss of both short- and long-term recognition memory. Histologically, obesity was associated with decreased neuronal density in the hippocampal DG and CA1 regions. Furthermore, hippocampal ROS was significantly elevated in the ZDF-HG group, and glutathione reductase activity was reduced in both obese phenotypes. Conclusions: The findings demonstrate that obesity initiates hippocampal neurodegeneration and motor decline, and that hyperglycemia severely impairs recognition memory. These results emphasize the critical interplay between metabolic dysfunction and cognitive decline, highlighting the necessity of managing both obesity and T2D to prevent early neurodegenerative changes. Full article
(This article belongs to the Special Issue Advances in Murine Models for Metabolic Diseases: Insights into Diabetes, Obesity, and Cardiovascular Conditions)
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21 pages, 4112 KB  
Article
Metabolic Characteristics of Schisantherin B in Mice with Metabolic-Associated Fatty Liver Disease
by Fei-Long Liu, Zhao-Rui Song, Meng Gao, Xi-Yuan Feng, Meng-Yang Wang, Zhi-Hong Zhang, He Li, Chun-Mei Wang and Jing-Hui Sun
Metabolites 2025, 15(12), 763; https://doi.org/10.3390/metabo15120763 - 25 Nov 2025
Viewed by 724
Abstract
Objectives: We aimed to observe the pharmacokinetic differences of schisantherin B (STB) in the blood and liver of normal and metabolic-associated fatty liver disease (MAFLD) mice, as well as the changes in CYP450 enzymes in MAFLD mice. Methods: A MAFLD model [...] Read more.
Objectives: We aimed to observe the pharmacokinetic differences of schisantherin B (STB) in the blood and liver of normal and metabolic-associated fatty liver disease (MAFLD) mice, as well as the changes in CYP450 enzymes in MAFLD mice. Methods: A MAFLD model was established in C57 mice fed a high-fat diet. Blood and liver samples from mice administered STB (5 mg/kg) were analyzed by high-performance liquid chromatography–electrospray tandem mass spectrometry (HPLC-ESI-MS) to identify major metabolites of STB and assess the activity of CYP450 enzymes. Pharmacokinetic parameters were calculated using DAS 3.0 software. The cocktail assay method was employed to determine CYP450 enzyme activity in hepatocytes in vitro. Results: The activities of CYP1A2, CYP2B6, CYP2C9, and CYP3A4 were significantly decreased, while the CYP2E1 activity was significantly increased in MAFLD hepatocyte model. In vitro liver microsomal experiments revealed that STB was primarily metabolized by CYP3A4 and CYP2C9. Compared to normal mice, STB in the liver tissue of MAFLD mice showed a significantly reduced area under the curve (AUC) and peak concentration (Cmax), prolonged half-life (t1/2), decreased mean retention time (MRT), and increased clearance (CL). In contrast, the AUC, Cmax, and t1/2 of STB in the serum of MAFLD mice were significantly increased, while the CL was decreased. Conclusions: Changes in the activity of liver microsomal enzymes following fatty liver injuries in MAFLD mice may lead to pharmacokinetic differences in STB, thereby affecting its metabolism in the liver. Full article
(This article belongs to the Special Issue Advances in Murine Models for Metabolic Diseases: Insights into Diabetes, Obesity, and Cardiovascular Conditions)
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9 pages, 1359 KB  
Article
Clay Attenuates Diarrhea Induced by Fat in a Mouse Model
by Shalom Emmanuel, Nyma Siddiqui, Ting Du, Eric Asare, Yuan Chen, Huan Xie, Dong Liang and Song Gao
Metabolites 2025, 15(7), 483; https://doi.org/10.3390/metabo15070483 - 17 Jul 2025
Viewed by 1432
Abstract
Background: Diarrhea induced by an excessive amount of fat is a prevalent gastrointestinal disorder. Currently, there are limited animal models and treatment options for diarrhea associated with fat. This study aims to develop a mouse model of high-fat-associated diarrhea using glyceryl-trioleate (GTO) and [...] Read more.
Background: Diarrhea induced by an excessive amount of fat is a prevalent gastrointestinal disorder. Currently, there are limited animal models and treatment options for diarrhea associated with fat. This study aims to develop a mouse model of high-fat-associated diarrhea using glyceryl-trioleate (GTO) and evaluate the potential of montmorillonite clay (MMT) in mitigating this condition. Methods: GTO was administered to mice at different doses through oral gavage to induce diarrhea. Clay was treated through oral gavage to evaluate its anti-diarrhea effect. Fecal conditions were monitored. Intestinal tissues were subjected to histological examination to assess structural integrity. The total fecal bile acids were evaluated using a bile acid assay kit to determine the mechanism of action. Results: The results showed that a diarrhea model was established by administering GTO at 2000 mg/kg. When the animals were treated with clay, diarrhea incidence and severity were decreased significantly in a dose-dependent manner. Compared to the untreated group receiving GTO alone, clay co-administration at 2000 mg/kg reduced diarrhea scores by approximately 48%, while the higher dose of 4000 mg/kg achieved an 83% reduction. Fecal bile acid analysis showed that diarrhea is associated with total bile acid levels in the feces. Histological exams showed that diarrhea is associated with tissue inflammation in the colon. Conclusions: This study showed that GTO administration induced diarrhea in mice, and clay effectively alleviates fat-induced diarrhea through modulation of fecal bile acid composition. These findings suggest that this model can be used to evaluate diarrhea associated with excessive amounts of fat and clay that can be further tested for diarrhea attenuation. Full article
(This article belongs to the Special Issue Advances in Murine Models for Metabolic Diseases: Insights into Diabetes, Obesity, and Cardiovascular Conditions)
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32 pages, 5153 KB  
Article
Naringenin Decreases Retroperitoneal Adiposity and Improves Metabolic Parameters in a Rat Model of Western Diet-Induced Obesity
by Gabriela López-Almada, J. Abraham Domínguez-Avila, Rosario Maribel Robles-Sánchez, Jonathan Arauz-Cabrera, Gustavo Martínez-Coronilla, Gustavo A. González-Aguilar and Norma Julieta Salazar-López
Metabolites 2025, 15(2), 109; https://doi.org/10.3390/metabo15020109 - 8 Feb 2025
Cited by 3 | Viewed by 2786
Abstract
Background: Obesity is a multifactorial disease with detrimental effects on health and quality of life; unregulated satiety plays a crucial role in food intake and obesity development. Naringenin (NAR) has shown beneficial effects on lipid and carbohydrate metabolism, although its impact on adiposity [...] Read more.
Background: Obesity is a multifactorial disease with detrimental effects on health and quality of life; unregulated satiety plays a crucial role in food intake and obesity development. Naringenin (NAR) has shown beneficial effects on lipid and carbohydrate metabolism, although its impact on adiposity and satiety remains unclear. This study reports a Western diet (WD)-induced obesity model in rats, wherein 100 mg/kg of NAR was administered as an anti-obesity agent for 8 weeks; oxidative stress, lipid profile, and satiety biomarkers were then studied, as well as in silico interaction between NAR and cholecystokinin (CCK) and ghrelin receptors. Results: NAR supplementation resulted in a significant decrease in retroperitoneal adipose tissue and liver weight, as compared to the untreated WD group (p < 0.05), potentially associated with a decreased feed efficiency. NAR also inhibited the development of dyslipidemia, particularly by reducing serum triglycerides (p < 0.05). NAR supplementation increased CCK serum levels in the basal diet group, an effect that was abolished by the WD (p < 0.05); likewise, no changes were determined on ghrelin (p > 0.05). In silico data shows that NAR is capable of interacting with the CCK and ghrelin receptors, which suggests a potential for it to modulate hunger/satiety signaling by interacting with them. Conclusions: We conclude that NAR has anti-obesogenic effects and may regulate CCK serum levels, although further research is still needed. Full article
(This article belongs to the Special Issue Advances in Murine Models for Metabolic Diseases: Insights into Diabetes, Obesity, and Cardiovascular Conditions)
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