Animal Models of Pancreatic Diseases

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 8548

Special Issue Editors


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Guest Editor
Department of Surgery, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
Interests: pancreas; type 1 diabetes; islet transplantation; immunology; immunotherapies; biochemistry

E-Mail Website
Guest Editor
Department of Surgery, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
Interests: kidney, pancreas and islet transplant; transplantation tolerance; gene therapy; xenotransplantation; transplant immunosuppression; pancreas

Special Issue Information

Dear Colleagues,

Animal models play a pivotal role in advancing our understanding of pancreatic diseases, including pancreatitis, pancreatic cancer and diabetes. These models, predominantly rodents, provide valuable insights into the etiology, pathogenesis and potential therapeutic interventions for these conditions. For example, in the context of pancreatitis, both acute and chronic forms have been replicated in rodents through methods such as cerulein administration or ethanol exposure. These studies have been instrumental in elucidating the inflammatory cascades and fibrotic changes observed in human pancreatitis and have helped identify potential therapeutic targets. In the realm of pancreatic cancer research, genetically engineered mouse models (GEMMs) simulate human pancreatic cancer development by introducing key mutations such as Kras, p53 and Smad4 mutations. This enables researchers to investigate various stages of tumor development, from initiation to metastasis. Additionally, xenograft and patient-derived xenograft (PDX) models, that involve the transplantation of human tumor cells or tissues into mice, provide invaluable platforms for testing novel anticancer therapies and personalized medicine approaches. In diabetes research, several animal models have been employed to study both type 1 and type 2 diabetes. For instance, the non-obese diabetic (NOD) mouse model has played a pivotal role in elucidating the autoimmune basis of type 1 diabetes. Chemically induced models, such as streptozotocin-treated rodents, closely mimic the beta-cell destruction characteristic of autoimmune diabetes, and have helped delineate underlying mechanisms, discover novel immunotherapies for promoting islet or pancreas graft survival, and identify potential regenerative therapies. Diet-induced obesity rodents and genetically modified mice (e.g., ob/ob and db/db) have been instrumental in replicating insulin resistance and obesity, key features of type 2 diabetes, and facilitating research on insulin signaling pathways and glucose metabolism. Animal models also serve as vital platforms for the preclinical testing of potential treatments, guiding therapeutic development and contributing to improved patient outcomes in pancreatic diseases. This Special Issue explores novel and diverse animal models used in pancreatic disease research, and highlights the key findings and contributions made to date. 

Dr. Preeti Chhabra
Dr. Kenneth Brayman
Guest Editors

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Keywords

  • animal models
  • pancreatic diseases
  • pancreatitis
  • pancreatic cancer
  • diabetes
  • pathogenesis
  • therapeutic targets
  • preclinical testing

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Published Papers (4 papers)

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Research

13 pages, 1921 KiB  
Article
Smad4 Heterozygous Knockout Effect on Pancreatic and Body Weight in F1 Population Using Collaborative Cross Lines
by Osayd Zohud, Iqbal M. Lone, Kareem Midlej, Aysar Nashef and Fuad A. Iraqi
Biology 2024, 13(11), 918; https://doi.org/10.3390/biology13110918 - 12 Nov 2024
Viewed by 976
Abstract
Smad4, a critical tumor suppressor gene, plays a significant role in pancreatic biology and tumorigenesis. Genetic background and sex are known to influence phenotypic outcomes, but their impact on pancreatic weight in Smad4-deficient mice remains unclear. This study investigates the impact [...] Read more.
Smad4, a critical tumor suppressor gene, plays a significant role in pancreatic biology and tumorigenesis. Genetic background and sex are known to influence phenotypic outcomes, but their impact on pancreatic weight in Smad4-deficient mice remains unclear. This study investigates the impact of Smad4 deficiency on pancreatic weight in first-generation (F1) mice from diverse collaborative cross (CC) lines, focusing on the influence of genetic background and sex. F1 mice were generated by crossbreeding female CC mice with C57BL/6J-Smad4tm1Mak males. Genotyping confirmed the presence of Smad4 knockout alleles. Mice were housed under standard conditions, euthanized at 80 weeks, and their pancreatic weights were measured, adjusted for body weight, and analyzed for effects of Smad4 deficiency, sex, and genetic background. The overall population of F1 mice showed a slight but non-significant increase in adjusted pancreatic weights in heterozygous knockout mice compared to wild-type mice. Sex-specific analysis revealed no significant difference in males but a significant increase in adjusted pancreatic weights in heterozygous knockout females. Genetic background analysis showed that lines CC018 and CC025 substantially increased adjusted pancreatic weights in heterozygous knockout mice. In contrast, other lines showed no significant difference or varied non-significant changes. The interplay between genetic background and sex further influenced these outcomes. Smad4 deficiency affects pancreatic weight in a manner significantly modulated by genetic background and sex. This study highlights the necessity of considering these factors in genetic research and therapeutic development, demonstrating the value of the collaborative cross mouse population in dissecting complex genetic interactions. Full article
(This article belongs to the Special Issue Animal Models of Pancreatic Diseases)
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16 pages, 9463 KiB  
Article
Schisandrin A Attenuates Diabetic Nephropathy via EGFR/AKT/GSK3β Signaling Pathway Based on Network Pharmacology and Experimental Validation
by Pengyu Wang, Qing Lan, Qi Huang, Ruyi Zhang, Shuo Zhang, Leiming Yang, Yan Song, Tong Wang, Guandi Ma, Xiufen Liu, Xiying Guo, Youzhi Zhang and Chao Liu
Biology 2024, 13(8), 597; https://doi.org/10.3390/biology13080597 - 8 Aug 2024
Cited by 3 | Viewed by 1936
Abstract
Diabetic nephropathy (DN) is one of the common complications of diabetes and the main cause of end-stage renal disease (ESRD) in clinical practice. Schisandrin A (Sch A) has multiple pharmacological activities, including inhibiting fibrosis, reducing apoptosis and oxidative stress, and regulating immunity, but [...] Read more.
Diabetic nephropathy (DN) is one of the common complications of diabetes and the main cause of end-stage renal disease (ESRD) in clinical practice. Schisandrin A (Sch A) has multiple pharmacological activities, including inhibiting fibrosis, reducing apoptosis and oxidative stress, and regulating immunity, but its pharmacological mechanism for the treatment of DN is still unclear. In vivo, streptozotocin (STZ) and a high-fat diet were used to induce type 2 diabetic rats, and Sch A was administered for 4 weeks. At the same time, protein–protein interaction (PPI) networks were established to analyze the overlapping genes of DN and Sch A. Subsequently, the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to determine the hub pathway. In addition, molecular docking was used to preliminarily verify the affinity of hub proteins and Sch A. Further, H&E staining, Sirius red staining, immunohistochemistry, immunofluorescence, and western blot analysis were used to detect the location and expression of related proteins in DN. This study revealed the multi-target and multi-pathway characteristics of Sch A in the treatment of DN. First, Sch A could effectively improve glucose tolerance, reduce urine microprotein and urine creatinine levels, and alleviate renal pathological damage in DN rats. Second, EGFR was the hub gene screened in overlapping genes (43) of Sch A (100) and DN (2524). Finally, it was revealed that Sch A could inhibit the protein expression levels of EGFR and PTRF and reduced the expression of apoptosis-related proteins, and this effect was related to the modulation of the AKT/GSK-3β signaling pathway. In summary, Sch A has a protective effect in DN rats, EGFR may be a potential therapeutic target, throughout modulating AKT/GSK-3β pathway. Full article
(This article belongs to the Special Issue Animal Models of Pancreatic Diseases)
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16 pages, 4590 KiB  
Article
Among Other Tissues, Short-Term Garlic Oral Treatment Incrementally Improves Indicants of Only Pancreatic Islets of Langerhans Histology and Insulin mRNA Transcription and Synthesis in Diabetic Rats
by Amani M. Al-Adsani and Khaled K. Al-Qattan
Biology 2024, 13(5), 355; https://doi.org/10.3390/biology13050355 - 18 May 2024
Cited by 3 | Viewed by 2190
Abstract
Background: The source, mRNA transcription, and synthesis of insulin in the pancreas, in addition to the bile duct and liver, in streptozotocin (STZ)-induced diabetic rats (DR) in response to garlic oral treatment are not yet clear. Objective: This study investigated the accumulative effects [...] Read more.
Background: The source, mRNA transcription, and synthesis of insulin in the pancreas, in addition to the bile duct and liver, in streptozotocin (STZ)-induced diabetic rats (DR) in response to garlic oral treatment are not yet clear. Objective: This study investigated the accumulative effects of continued garlic oral treatment on changes in the pancreas, bile duct, and liver with regards to: 1—Insulin mRNA transcription, synthesis, and concentration in relation to changes in serum insulin (SI); 2—Insulinogenic cells insulin intensity and distribution, proliferation, and morphology. Method: Fasting blood glucose (FBG) and insulin concentration in serum and pancreas (PI) and sources and mRNA transcription in the pancreas, bile duct, and liver in normal rats given normal saline (NR-NS) and DR given either NS (DR-NS) or garlic extract (DR-GE) before and after 1, 4, and 8 weeks of oral treatment were examined. Results: Compared to NR-NS, DR-NS showed a significant increase in FBG and reductions in SI and PI and deterioration in islets histology, associated pancreatic insulin numerical intensities, and mRNA transcription. However, compared to DR-NS, the targeted biochemical, histological, and genetic variables of DR-GE were significantly and incrementally improved as garlic treatment continued. Insulin or its indicators were not detected either in the bile duct or the liver in DR-GE. Conclusions: 8 weeks of garlic oral treatment is enough to incrementally restore only pancreatic islets of Langerhans insulin intensity and insulinogenic cells proliferation, morphology, and distribution. These indices were associated with enhanced pancreatic insulin mRNA transcription and synthesis. Eight weeks of garlic treatment were not enough to stimulate insulinogenesis in either the bile duct or the liver. Full article
(This article belongs to the Special Issue Animal Models of Pancreatic Diseases)
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14 pages, 5747 KiB  
Article
Mesenchymal Stem Cell-Derived Exosomes Loaded with Selenium or Nano Selenium as a Novel Therapeutic Paradigm for Streptozotocin-Induced Type 1 Diabetes in Rats
by Dlovan Y. Khalil, Ridah H. Hussein and Wafaa M. El-Kholy
Biology 2024, 13(4), 253; https://doi.org/10.3390/biology13040253 - 11 Apr 2024
Cited by 1 | Viewed by 2484
Abstract
Type 1 diabetes mellitus (T1DM) is a metabolic disorder characterized by hyperglycemia due to insulin insufficiency as a consequence of the pancreatic β-cells’ auto-immune attack. Nowadays, the application of mesenchymal stem cell-derived exosomes (MSCs-Exs) as the main cell-free therapy for diabetes treatment is [...] Read more.
Type 1 diabetes mellitus (T1DM) is a metabolic disorder characterized by hyperglycemia due to insulin insufficiency as a consequence of the pancreatic β-cells’ auto-immune attack. Nowadays, the application of mesenchymal stem cell-derived exosomes (MSCs-Exs) as the main cell-free therapy for diabetes treatment is becoming more and more extensive. In non-autologous therapy, researchers are moving towards a new strategy based on loading MSC-Exs with certain drugs, aimed at maintaining and maximizing the function of exosomes at the function site and enhancing their efficiency and safety. This study aims to explore and compare the therapeutic potentialities of mesenchymal stem cell-derived exosomes (MSCs-Exs) loaded with either selenium (Se) or nano selenium (NSe), a natural antioxidant micronutrient, in the management of T1DM in rats. In our 4-week experiment, six rat groups were included, namely, control, Ex+Se, Ex+NSe, STZ-diabetic (D), D+ Ex+Se, and D+Ex+NSe groups. Both diabetic-treated groups showed marked pancreatic regenerative antioxidant, immunomodulatory, anti-inflammatory, and anti-apoptotic capacities, with the D+Ex+NSe injection showing superiority in managing diabetes hazards, as evidenced by various biochemical and histological assessments. Full article
(This article belongs to the Special Issue Animal Models of Pancreatic Diseases)
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