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Biology
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Animal Models of Metabolic Diseases
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Animal Models of Metabolic Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1670

Special Issue Editors

Prof. Dr. Júlio Cezar De Oliveira

E-Mail Website
Guest Editor
Institute of Health Sciences (ICS), Federal University of Mato Grosso (UFMT), Sinop 78550-728, MT, Brazil
Interests: metabolic dysfunction; developmental origins of health and diseases (DOHaD); nutritional insults; undernutrition; obesity; intrauterine, breastfeeding and adolescence
Prof. Dr. Melvin Khee Shing Leow

E-Mail Website
Guest Editor
Clinical Nutrition Research Centre (CNRC), Singapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A*STAR) and National University Health System, Singapore 117599, Singapore
Interests: diabetes; metabolic physiology; adipocyte biology; math modeling; thyroidology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit an original article or a review article for this Special Issue, titled “Animal Models of Metabolic Diseases”.

Metabolic diseases constitute a cluster of disorders that, in general, have background multifactorial causes, which make them a growing health problem worldwide today. To understand the process involved in the origin, progress and therapeutical approaches are pivotal to most efficiently contribute, alongside new strategies on improving human health.

In the field of metabolic dysfunction, over the years, several animal models have been used by researchers worldwide to put out scientific evidence that could favor a better understanding of the mechanisms, pathophysiology, and strategies to mitigate metabolic diseases (type 2 diabetes mellitus, hypertension, obesity, and its associated comorbidities, among others). Descriptions of these animal models, in this field, are not yet ideal, and do not converging to create the perfect animal model. However, this compounds a precious source that can be used for translating knowledge about new strategies for improving human metabolic health.

Among many animal models, those of monogenic animals seem to be the best choice for use if a single aspect of the metabolic disruption is being considered. In addition, different animal models of induced metabolic impairments (e.g., high-fat-diet-induced obesity; models of diabetes induced by streptozotocin, alloxan, supraphysiological dexamethasone administration, and others, such as those including the long-term metabolic consequences associated with insult and exposure during critical stages of life development) are more representative of real human conditions, since metabolic diseases display multifactorial origins, including the influence of environmental agents on gene expression patterns.

This Special Issue aims to bring together studies on animal models of metabolic diseases, focusing on the mechanisms and pathophysiology of metabolic diseases, as well as studies on therapeutical strategies in this field.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but need not be limited to) studies with animal models reporting on the pathophysiology and/or mechanisms of origins and/or progression, as well as strategies of the treatment and/or prevention of metabolic diseases, such as the following:

  • Type 2 diabetes mellitus.
  • Obesity.
  • Hypertension.
  • Nonalcoholic fatty liver disease (NAFLD).
  • Long-term metabolic diseases (into the paradigm of Developmental Origins of Health and Diseases, DOHaD).

We look forward to receiving your contributions.

Prof. Dr. Júlio Cezar De Oliveira
Prof. Dr. Melvin Khee Shing Leow
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. Biology 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

  • experimental models
  • metabolic syndrome
  • insulin resistance
  • type 2 diabetes mellitus
  • obesity
  • dyslipidemia
  • hypertension
  • metabolic programming
  • DOHaD

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Published Papers (4 papers)

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Research

17 pages, 6793 KiB  
Article
Anti-Diabetic and Antioxidant Effect Evaluation of Thai Shallot and Cha-Miang in Diabetic Rats
by Jiraporn Laoung-on, Artorn Anuduang, Chalermpong Saenjum, Kittipan Rerkasem, Somdet Srichairatanakool, Kongsak Boonyapranai and Sakaewan Ounjaijean
Biology 2025, 14(6), 627; https://doi.org/10.3390/biology14060627 - 29 May 2025
Abstract
Background: Type 2 diabetes mellitus is a chronic metabolic disease related to obesity and high-calorie diets, which presents hyperglycemia and insulin resistance. The management of diabetes can cause a rise in financial burden and synthetic medications can have adverse effects. This study aims [...] Read more.
Background: Type 2 diabetes mellitus is a chronic metabolic disease related to obesity and high-calorie diets, which presents hyperglycemia and insulin resistance. The management of diabetes can cause a rise in financial burden and synthetic medications can have adverse effects. This study aims to investigate the anti-diabetic and antioxidant activity of SHE, CME, and SHE in diabetic rats. Methods: Seventy-eight rats were randomly assigned to the following 13 groups (n = 6): N-DW, D-DW, D-M, D-S, D-C, D-F, D-SC, D-SF, D-SM, D-CM, D-FM, D-SCM, and D-SFM, for 8 weeks. Body weight, relative organ weight, blood glucose, insulin resistance, and plasma biomarkers related to diabetes were determined. Results: Diabetic rats had a significantly decreased body weight, RBC-GHS, liver-GHS, and RBC-SOD activity and a significantly increased relative organ weight, blood glucose levels, insulin levels, insulin resistance, HbA1C, TC, TG, LDL, plasma-MDA, and liver-MDA when compared to the N-DW group. However, plant supplementation and metformin improved diabetes-related parameters, especially the combination of CME or FCME with SHE and metformin, which showed the greatest potential for improving diabetic conditions. (4) Conclusions: The research indicates that CME or FCME conjugated with SHE and metformin demonstrates the greatest potential for enhancing diabetic conditions, confirming positive synergism. These findings suggest that the combination of CME or FCME with SHE and metformin may be effective for diabetic treatment. Full article
(This article belongs to the Special Issue Animal Models of Metabolic Diseases)
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16 pages, 2651 KiB  
Article
Comparative Analysis of Letrozole and Estradiol Valerate PCOS Models: Reproductive and Metabolic Outcomes with and Without High-Fat Diet
by Xóchitl Acuña Escalona, Rocio Sarahy Ayala, Karla Cortez, Sophie Fernández Sánchez, Teresa Tomé-Dehesa, Verónica Díaz-Hernández, Carlos Larqué and Rene Escalona
Biology 2025, 14(6), 592; https://doi.org/10.3390/biology14060592 - 23 May 2025
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Abstract
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in reproductive-aged women, characterized by hyperandrogenism, oligoanovulation, and polycystic ovarian morphology. Despite its classification as a reproductive disorder, PCOS is closely associated with metabolic dysregulation, including insulin resistance and obesity. An ideal animal model [...] Read more.
Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in reproductive-aged women, characterized by hyperandrogenism, oligoanovulation, and polycystic ovarian morphology. Despite its classification as a reproductive disorder, PCOS is closely associated with metabolic dysregulation, including insulin resistance and obesity. An ideal animal model for PCOS should replicate both reproductive and metabolic features of the condition. In this study, we compared two widely used postnatal PCOS models (letrozole and estradiol valerate [EV]) administered alone or in combination with a high-fat diet (HFD), assessing their ability to induce both the reproductive and metabolic features. Letrozole treatment led to significant weight gain and increased visceral adiposity, effects that were amplified by HFD. Conversely, EV treatment showed a tendency toward reduced body mass. While neither model significantly altered fasting glucose levels, letrozole combined with HFD impaired glucose tolerance, supporting its role in metabolic dysfunction. Hyperandrogenism was more consistently induced by letrozole compared to EV, aligning with clinical PCOS phenotypes. Both treatments disrupted estrous cyclicity and induced polycystic ovarian morphology, though metabolic disturbances were more pronounced in the letrozole model. These findings suggest that letrozole, particularly in combination with HFD, provides a more consistent model for studying both the reproductive and metabolic facets of PCOS. Full article
(This article belongs to the Special Issue Animal Models of Metabolic Diseases)
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16 pages, 2783 KiB  
Article
Transdermal Semaglutide Administration in Mice: Reduces Body Weight by Suppressing Appetite and Enhancing Metabolic Rate
by Wenjing Li, Ruilin Cai, Binxin Yin, Yingying Zhou, Xinyuan Dong, Wenting Li and Jing Wen
Biology 2025, 14(5), 575; https://doi.org/10.3390/biology14050575 - 20 May 2025
Viewed by 173
Abstract
Background: Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that shows significant efficacy in treating obesity. However, its associated side effects, including poor patient compliance and gastrointestinal inflammation, are concerning and may be largely attributed to its administration methods (e.g., injection vs. oral) [...] Read more.
Background: Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that shows significant efficacy in treating obesity. However, its associated side effects, including poor patient compliance and gastrointestinal inflammation, are concerning and may be largely attributed to its administration methods (e.g., injection vs. oral) and the pronounced fluctuations in systemic drug concentrations. To address these challenges, we investigated an innovative drug delivery system (Transdermal Drug Delivery System, TDDS) designed to maintain therapeutic efficacy while improving patient adherence. Results: Both transdermal and injection treatments of semaglutide decreased body weight, carcass weight, blood glucose, and triglyceride levels in male mice compared with the vehicle-treated control group. In addition, transdermal semaglutide in mice reduced the expression of feeding neuropeptides and the mass of the digestive tract, but increased brown adipose tissue (BAT) mass, metabolic rate, and physical activity, compared with the semaglutide injection group. Additionally, transdermal semaglutide had anxiolytic effects on behavior and did not alter tissue pathology in mice. Conclusion: Compared with the injection paradigm, transdermal semaglutide treatment achieved superior weight loss results in two possible ways: It may reduce energy intake by decreasing the expression of feeding neuropeptides and reducing the weight of the digestive tract. It may also facilitate energy expenditure by enhancing physical activity and increasing BAT mass to boost the metabolic rate. Transdermal semaglutide treatment also has an anxiolytic effect on behavior. Together, our data suggest that TDDS treatment of GLP-1RA may have superior clinical safety and sustainability, providing a novel, efficient, and low-risk obesity treatment. Full article
(This article belongs to the Special Issue Animal Models of Metabolic Diseases)
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14 pages, 2321 KiB  
Article
Maternal AGE Precursors During Lactation Alters Offspring Glycemic Homeostasis Early in Life
by Lucas P. J. Saavedra, Flávio A. Francisco, Scarlett R. Raposo, Keilah V. N. Cavalcante, Nilza C. Buttow, Stephanie C. Borges, Rodrigo M. Gomes, Hericles M. Campos, Gessica D. Gonçalves, Silvano Piovan, Paulo C. Ghedini, Kelly V. Prates, Ananda Malta, Paulo Matafome, Paulo C. F. Mathias and Douglas L. Almeida
Biology 2025, 14(2), 160; https://doi.org/10.3390/biology14020160 - 5 Feb 2025
Viewed by 837
Abstract
Background: Advanced glycation end-products (AGEs) are linked to the development of oxidative stress, insulin resistance, and impaired insulin secretion. Adverse early life conditions, such as exposure to AGEs and their precursors, may lead offspring to the development of metabolic dysfunction in adulthood. Nonetheless, [...] Read more.
Background: Advanced glycation end-products (AGEs) are linked to the development of oxidative stress, insulin resistance, and impaired insulin secretion. Adverse early life conditions, such as exposure to AGEs and their precursors, may lead offspring to the development of metabolic dysfunction in adulthood. Nonetheless, the early impact in offspring metabolism by maternal intake of AGEs precursors during lactation is not known. Objective: Investigate early life metabolism of the offspring whose breastfeeding dams were orally exposed to AGEs precursor. Methods: Breastfeeding Wistar rats were daily treated with the glycation precursor methylglyoxal (MG—60 mg/kg of bodyweight) by gavage or saline 0.9% control (CO) until weaning. In vivo glycemic homeostasis in male offspring was assessed, followed by euthanasia for tissue sample collection for ex vivo assessments. Results: At weaning, MG offspring presented decreased bodyweight (p < 0.05), perigonadal (p < 0.01) and retroperitoneal (p < 0.01) fat. MG offspring presented decreased glucose tolerance (p < 0.05), lower basal insulinemia (p < 0.001), reduced high-glucose static insulin secretion (p < 0.05), and reduced pancreatic islet area (p < 0.05). Accordingly, MG offspring pancreas showed lower GSH and SOD activity (p < 0.05; p < 0.001, respectively) and increased MPO (p < 0.05) activity. Conclusions: The consumption of AGE precursors by breastfeeding dams impaired offspring pancreatic function and glycemic homeostasis early in life. Full article
(This article belongs to the Special Issue Animal Models of Metabolic Diseases)
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