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Journal articles on the topic 'BTBR mice'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Flowers, Jessica B., Angie T. Oler, Samuel T. Nadler, et al. "Abdominal obesity in BTBR male mice is associated with peripheral but not hepatic insulin resistance." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (2007): E936—E945. http://dx.doi.org/10.1152/ajpendo.00370.2006.

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Insulin resistance is a common feature of obesity. BTBR mice have more fat mass than most other inbred mouse strains. On a chow diet, BTBR mice have elevated insulin levels relative to the C57BL/6J (B6) strain. Male F1 progeny of a B6 × BTBR cross are insulin resistant. Previously, we reported insulin resistance in isolated muscle and in isolated adipocytes in this strain. Whereas the muscle insulin resistance was observed only in male F1 mice, adipocyte insulin resistance was also present in male BTBR mice. We examined in vivo mechanisms of insulin resistance with the hyperinsulinemic euglyce

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Rozhkova, I. N., S. V. Okotrub, E. Yu Brusentsev, et al. "Effects of Assisted Reproductive Technologies on Social Behavior of BTBR Mice – A Model of Autism Spectrum Disorder." Российский физиологический журнал им И М Сеченова 109, no. 3 (2023): 315–33. http://dx.doi.org/10.31857/s0869813923030044.

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The present work is the first attempt to study the effect of such assisted reproductive technologies (ARTs), as in vitro culture of preimplantation embryos on the social behavior of offspring, using BTBR mice (BTBR T+Itpr3tf/J) as an idiopathic model of a-utism. The C57BL/6J mice were used as controls. Social behavior was studied in adult offspring mice obtained after in vitro culture and embryo transfer (ET) (groups ET-C57BL/6J and ET-BTBR). The BTBR mice demonstrated the reduced levels of social recognition and affiliation compared to C57BL/6J mice. The social affiliation and recognition tes

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Rezzani, Rita, Marzia Gianò, Daniela Pinto, Fabio Rinaldi, Cornelis J. F. van Noorden, and Gaia Favero. "Hepatic Alterations in a BTBR T + Itpr3tf/J Mouse Model of Autism and Improvement Using Melatonin via Mitigation Oxidative Stress, Inflammation and Ferroptosis." International Journal of Molecular Sciences 25, no. 2 (2024): 1086. http://dx.doi.org/10.3390/ijms25021086.

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Autism spectrum disorder (ASD) is a complicated neurodevelopmental disorder, and its etiology is not well understood. It is known that genetic and nongenetic factors determine alterations in several organs, such as the liver, in individuals with this disorder. The aims of the present study were to analyze morphological and biological alterations in the liver of an autistic mouse model, BTBR T + Itpr3tf/J (BTBR) mice, and to identify therapeutic strategies for alleviating hepatic impairments using melatonin administration. We studied hepatic cytoarchitecture, oxidative stress, inflammation and

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Anderson, Jacqueline M., Amber A. Boardman, Rhiannon Bates, Xunchang Zou, Wei Huang, and Lei Cao. "Hypothalamic TrkB.FL overexpression improves metabolic outcomes in the BTBR mouse model of autism." PLOS ONE 18, no. 3 (2023): e0282566. http://dx.doi.org/10.1371/journal.pone.0282566.

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BTBR T+ Itpr3tf/J (BTBR) mice are used as a model of autism spectrum disorder (ASD), displaying similar behavioral and physiological deficits observed in patients with ASD. Our recent study found that implementation of an enriched environment (EE) in BTBR mice improved metabolic and behavioral outcomes. Brain-derived neurotrophic factor (Bdnf) and its receptor tropomyosin kinase receptor B (Ntrk2) were upregulated in the hypothalamus, hippocampus, and amygdala by implementing EE in BTBR mice, suggesting that BDNF-TrkB signaling plays a role in the EE-BTBR phenotype. Here, we used an adeno-asso

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Kiffmeyer, Elizabeth A., Jameson A. Cosgrove, Jenna K. Siganos, et al. "Deficits in Cerebellum-Dependent Learning and Cerebellar Morphology in Male and Female BTBR Autism Model Mice." NeuroSci 3, no. 4 (2022): 624–44. http://dx.doi.org/10.3390/neurosci3040045.

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Recently, there has been increased interest in the role of the cerebellum in autism spectrum disorder (ASD). To better understand the pathophysiological role of the cerebellum in ASD, it is necessary to have a variety of mouse models that have face validity for cerebellar disruption in humans. Here, we add to the literature on the cerebellum in mouse models of autism with the characterization of the cerebellum in the idiopathic BTBR T + Itpr3tf/J (BTBR) inbred mouse strain, which has behavioral phenotypes that are reminiscent of ASD in patients. When we examined both male and female BTBR mice

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Kisaretova, Polina, Anton Tsybko, Natalia Bondar, and Vasiliy Reshetnikov. "Molecular Abnormalities in BTBR Mice and Their Relevance to Schizophrenia and Autism Spectrum Disorders: An Overview of Transcriptomic and Proteomic Studies." Biomedicines 11, no. 2 (2023): 289. http://dx.doi.org/10.3390/biomedicines11020289.

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Animal models of psychopathologies are of exceptional interest for neurobiologists because these models allow us to clarify molecular mechanisms underlying the pathologies. One such model is the inbred BTBR strain of mice, which is characterized by behavioral, neuroanatomical, and physiological hallmarks of schizophrenia (SCZ) and autism spectrum disorders (ASDs). Despite the active use of BTBR mice as a model object, the understanding of the molecular features of this strain that cause the observed behavioral phenotype remains insufficient. Here, we analyzed recently published data from indep

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Ghaderzadeh, Sadaf, Baiyeendang Agbor-Baiyee, Chidera Obiwuma, et al. "395 Systemic Administration of miR-451 Improves Autophagy Response in an Accelerated Mouse Model of Diabetic Kidney Disease." Journal of Clinical and Translational Science 8, s1 (2024): 118. http://dx.doi.org/10.1017/cts.2024.345.

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OBJECTIVES/GOALS: Diabetic Kidney Disease (DKD) is a common diabetes complication, often linked to end-stage renal disease in the United States (US). While autophagy and miRNAs are pivotal, miR-451’s specific role remains understudied. Our study explores its renoprotective effects in an accelerated DKD mouse model. METHODS/STUDY POPULATION: We assessed the effect of miR-451 mimic treatment on Diabetic Kidney Disease (DKD) in BTBR ob/ob mice, known for their rapid DKD-like renal lesions. Mice were divided into four groups: WT (wild-type), BTBR ob/ob, WT+miR-451 (wild-type with miR-451 mimic), a

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Opazo-Ríos, Lucas, Manuel Soto-Catalán, Iolanda Lázaro, et al. "Meta-Inflammation and De Novo Lipogenesis Markers Are Involved in Metabolic Associated Fatty Liver Disease Progression in BTBR ob/ob Mice." International Journal of Molecular Sciences 23, no. 7 (2022): 3965. http://dx.doi.org/10.3390/ijms23073965.

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Metabolic associated fatty liver disease (MAFLD) is a hepatic manifestation of metabolic syndrome and usually associated with obesity and diabetes. Our aim is to characterize the pathophysiological mechanism involved in MAFLD development in Black Tan and brachyuric (BTBR) insulin-resistant mice in combination with leptin deficiency (ob/ob). We studied liver morphology and biochemistry on our diabetic and obese mice model (BTBR ob/ob) as well as a diabetic non-obese control (BTBR + streptozotocin) and non-diabetic control mice (BTBR wild type) from 4–22 weeks. Lipid composition was assessed, an

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Tordoff, Michael G., and Hillary T. Ellis. "Taste dysfunction in BTBR mice due to a mutation of Itpr3, the inositol triphosphate receptor 3 gene." Physiological Genomics 45, no. 18 (2013): 834–55. http://dx.doi.org/10.1152/physiolgenomics.00092.2013.

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The BTBR T+ tf/J (BTBR) mouse strain is indifferent to exemplars of sweet, Polycose, umami, bitter, and calcium tastes, which share in common transduction by G protein-coupled receptors (GPCRs). To investigate the genetic basis for this taste dysfunction, we screened 610 BTBR × NZW/LacJ F2 hybrids, identified a potent QTL on chromosome 17, and isolated this in a congenic strain. Mice carrying the BTBR/BTBR haplotype in the 0.8-Mb (21-gene) congenic region were indifferent to sweet, Polycose, umami, bitter, and calcium tastes. To assess the contribution of a likely causative culprit, Itpr3, the

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Gembardt, Florian, Christoph Bartaun, Natalia Jarzebska, et al. "The SGLT2 inhibitor empagliflozin ameliorates early features of diabetic nephropathy in BTBR ob/ob type 2 diabetic mice with and without hypertension." American Journal of Physiology-Renal Physiology 307, no. 3 (2014): F317—F325. http://dx.doi.org/10.1152/ajprenal.00145.2014.

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Diabetic nephropathy is the leading cause of end-stage renal disease in humans in the Western world. The recent development of Na+-glucose cotransporter 2 (SGLT2) inhibitors offers a new antidiabetic therapy via enhanced glucose excretion. Whether this strategy exerts beneficial effects on the development of type 2 diabetic nephropathy is still largely unclear. We investigated the effects of the specific SGLT2 inhibitor empagliflozin in BTBR.Cg-Lep<ob>/WiscJ (BTBR ob/ ob) mice, which spontaneously develop type 2 diabetic nephropathy. In the first experiment, BTBR ob/ ob mice received eit

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Cominelli, Giorgia, Claudio Lonati, Daniela Pinto, et al. "Melatonin Attenuates Ferritinophagy/Ferroptosis by Acting on Autophagy in the Liver of an Autistic Mouse Model BTBR T+Itpr3tf/J." International Journal of Molecular Sciences 25, no. 23 (2024): 12598. http://dx.doi.org/10.3390/ijms252312598.

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Autism spectrum disorders (ASDs) are a pool of neurodevelopment disorders in which social impairment is the main symptom. Presently, there are no definitive medications to cure the symptoms but the therapeutic strategies that are taken ameliorate them. The purpose of this study was to investigate the effects of melatonin (MLT) in treating ASDs using an autistic mouse model BTBR T+Itpr3tf/J (BTBR). We evaluated the hepatic cytoarchitecture and some markers of autophagy, ferritinophagy/ferroptosis, in BTBR mice treated and not-treated with MLT. The hepatic morphology and the autophagy and ferrit

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Xiaoyan, Huang, Yang Zhaoxi, Zhang Lingli, Chen Jinyuan, and Qin Wen. "Taurine Improved Autism-Like Behaviours and Defective Neurogenesis of the Hippocampus in BTBR Mice through the PTEN/mTOR/AKT Signalling Pathway." Folia Biologica 70, no. 1 (2024): 45–52. http://dx.doi.org/10.14712/fb2024070010045.

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Effective treatment of patients with autism spectrum disorder (ASD) is still absent so far. Taurine exhibits therapeutic effects towards the autism-like behaviour in ASD model animals. Here, we determined the mechanism of taurine effect on hippocampal neurogenesis in genetically inbred BTBR T+ tf/J (BTBR) mice, a proposed model of ASD. In this ASD mouse model, we explored the effect of oral taurine supplementation on ASD-like behaviours in an open field test, elevated plus maze, marble burying test, self-grooming test, and three-chamber test. The mice were divided into four groups of normal co

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Abdavinejad, Sevda, Payton Charlton, and Micheal Dent. "Ultrasonic vocalizations produced by a mouse model of autism spectrum disorder differ following social experience." Journal of the Acoustical Society of America 156, no. 4_Supplement (2024): A86. https://doi.org/10.1121/10.0035196.

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Mice are highly effective models for studying neurodevelopmental disorders characterized by abnormal social behaviors, such as Autism Spectrum Disorder (ASD). Because mice produce Ultrasonic Vocalizations (USVs) with many features like human speech, they have been proposed as a model for investigating neurodevelopmental disorders characterized by impairments in social communication, including ASD. The BTBR T+T+Itpr3tf/J mouse is an inbred strain displaying social abnormalities, communication deficits, and repetitive behaviors analogous to the behavioral symptoms of ASD. Here, we investigate th

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Athnaiel, Onella, Greeshma A. Job, Roberto Ocampo, Pamela Teneqexhi, William S. Messer, and Michael E. Ragozzino. "Effects of the Partial M1 Muscarinic Cholinergic Receptor Agonist CDD-0102A on Stereotyped Motor Behaviors and Reversal Learning in the BTBR Mouse Model of Autism." International Journal of Neuropsychopharmacology 25, no. 1 (2021): 64–74. http://dx.doi.org/10.1093/ijnp/pyab079.

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Abstract Background Autism spectrum disorders (ASD) are a set of neurodevelopmental disorders marked by a lack of social interaction, restrictive interests, and repetitive behaviors. There is a paucity of pharmacological treatments to reduce core ASD symptoms. Various lines of evidence indicate that reduced brain muscarinic cholinergic receptor activity may contribute to an ASD phenotype. Methods The present experiments examined whether the partial M1 muscarinic receptor agonist, 5-(3-ethyl-1,2,4-oxadiazol-5-yl)-1,4,5,6-tetrahydropyrimidine hydrochloride (CDD-0102A), alleviates behavioral flex

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Rabaglia, Mary E., Mark P. Gray-Keller, Brian L. Frey, Michael R. Shortreed, Lloyd M. Smith та Alan D. Attie. "α-Ketoisocaproate-induced hypersecretion of insulin by islets from diabetes-susceptible mice". American Journal of Physiology-Endocrinology and Metabolism 289, № 2 (2005): E218—E224. http://dx.doi.org/10.1152/ajpendo.00573.2004.

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Most patients at risk for developing type 2 diabetes are hyperinsulinemic. Hyperinsulinemia may be a response to insulin resistance, but another possible abnormality is insulin hypersecretion. BTBR mice are insulin resistant and hyperinsulinemic. When the leptin ob mutation is introgressed into BTBR mice, they develop severe diabetes. We compared the responsiveness of lean B6 and BTBR mouse islets to various insulin secretagogues. The transamination product of leucine, α-ketoisocaproate (KIC), elicited a dramatic insulin secretory response in BTBR islets. The KIC response was blocked by methyl

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Ghaderzadeh, Sadaf, Baiyeendang Agbor-Baiyee, Chidera Obiwuma, Neal Mohit, Kanwal K. Gambhir, and Maurice B. Fluitt. "36 Kidney MiRNA expression in BTBR ob/ob mice at a critical time point in disease development and progression." Journal of Clinical and Translational Science 9, s1 (2025): 12–13. https://doi.org/10.1017/cts.2024.724.

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Objectives/Goals: Diabetic kidney disease (DKD) affects 40% of diabetic patients, leading to renal failure, yet the molecular drivers remain elusive. MicroRNAs, noncoding regulators of gene expression, may hold the key. This study aims to identify key miRNAs in DKD, providing crucial insights for early intervention. Methods/Study Population: miRNA sequencing was conducted on kidneys from 8-week old male BTBR wild type and BTBR ob/ob mice. BTBR ob/ob mice lack the hormone leptin and spontaneously develop type 2 diabetes, with morphological renal lesions characteristic of human DKD. Total RNA wa

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Alhosaini, Khaled, Mushtaq A. Ansari, Ahmed Nadeem, et al. "5-Aminoisoquinolinone, a PARP-1 Inhibitor, Ameliorates Immune Abnormalities through Upregulation of Anti-Inflammatory and Downregulation of Inflammatory Parameters in T Cells of BTBR Mouse Model of Autism." Brain Sciences 11, no. 2 (2021): 249. http://dx.doi.org/10.3390/brainsci11020249.

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Autism spectrum disorder (ASD) covers a range of neurodevelopmental disorders involving impairments in communication and repetitive and stereotyped patterns of behavior and reciprocal social interaction. 5-Aminoisoquinolinone (5-AIQ), a PARP-1 inhibitor, has neuroprotective and anti-inflammatory effects. We investigated the influence of 5-AIQ-treatment in BTBR T+ Itpr3tf/J (BTBR) mice as an autism model and used flow cytometry to assess the effect of 5-AIQ on FOXP3, Helios, GATA3, IL-9, IL-10 and IL-17A production by CXCR6+ and CD4+ T cells in the spleen. We also confirmed the effect of 5-AIQ

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Mutovina, Anastasia, Kseniya Ayriyants, Eva Mezhlumyan, et al. "Unique Features of the Immune Response in BTBR Mice." International Journal of Molecular Sciences 23, no. 24 (2022): 15577. http://dx.doi.org/10.3390/ijms232415577.

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Inflammation plays a considerable role in the pathogenesis of many diseases, including neurodegenerative and psychiatric ones. Elucidation of the specific features of an immune response in various model organisms, and studying the relation of these features with the behavioral phenotype, can improve the understanding of the molecular mechanisms of many psychopathologies. In this work, we focused on BTBR mice, which have a pronounced autism-like behavioral phenotype, elevated levels of oxidative-stress markers, an abnormal immune response, several structural aberrations in the brain, and other

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Fink, Lisbeth, Carsten Gotfredsen, Alexander Rosendahl, and Maiken Pedersen. "The kidney myeloid cell compartment is perturbed in diabetic BTBR ob/ob mice (INC6P.338)." Journal of Immunology 192, no. 1_Supplement (2014): 121.5. http://dx.doi.org/10.4049/jimmunol.192.supp.121.5.

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Abstract The BTBR ob/ob mouse is gaining interest as a model of diabetic nephropathy, because it develops progressive albuminuria and, as opposed to the db/db diabetic mouse, is considered to develop fibrotic kidney lesions. The mouse kidney contains multiple types of resident mononuclear phagocytes and neutrophils. In the Akita type 1 diabetes mouse model, macrophage recruitment has been shown to be a key driver of the diabetic nephropathy, and human diabetic nephropathy kidney specimens display increased macrophage infiltration. We aimed to study the myeloid cell populations locally in the B

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Alshammari, Musaad A., Mohammad R. Khan, Fawaz Alasmari, et al. "Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model." Neural Plasticity 2019 (December 17, 2019): 1–12. http://dx.doi.org/10.1155/2019/4893103.

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The axon initial segment (AIS), the site of action potential initiation in neurons, is a critical determinant of neuronal excitability. Growing evidence indicates that appropriate recruitment of the AIS macrocomplex is essential for synchronized firing. However, disruption of the AIS structure is linked to the etiology of multiple disorders, including autism spectrum disorder (ASD), a condition characterized by deficits in social communication, stereotyped behaviors, and very limited interests. To date, a complete understanding of the molecular components that underlie the AIS in ASD has remai

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Eissa, Nermin, Petrilla Jayaprakash, Holger Stark, Dorota Łażewska, Katarzyna Kieć-Kononowicz, and Bassem Sadek. "Simultaneous Blockade of Histamine H3 Receptors and Inhibition of Acetylcholine Esterase Alleviate Autistic-Like Behaviors in BTBR T+ tf/J Mouse Model of Autism." Biomolecules 10, no. 9 (2020): 1251. http://dx.doi.org/10.3390/biom10091251.

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Autism spectrum disorder (ASD) is a heterogenous neurodevelopmental disorder defined by persistent deficits in social interaction and the presence of patterns of repetitive and restricted behaviors. The central neurotransmitters histamine (HA) and acetylcholine (ACh) play pleiotropic roles in physiological brain functions that include the maintenance of wakefulness, depression, schizophrenia, epilepsy, anxiety and narcolepsy, all of which are found to be comorbid with ASD. Therefore, the palliative effects of subchronic systemic treatment using the multiple-active test compound E100 with high

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Nadler, Samuel T., Jonathan P. Stoehr, Mary E. Rabaglia, Kathryn L. Schueler, Morris J. Birnbaum, and Alan D. Attie. "Normal Akt/PKB with reduced PI3K activation in insulin-resistant mice." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (2001): E1249—E1254. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1249.

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Insulin stimulates muscle and adipose tissue to absorb glucose through a signaling cascade that is incompletely understood. Insulin resistance, the inability of insulin to appropriately stimulate glucose uptake, is a hallmark of type 2 diabetes mellitus. The development of experimental systems that model human insulin resistance is important in elucidating the defects responsible for the development of type 2 diabetes. When two strains of mice, BTBR and C57BL/6J (B6), are crossed, the resultant male offspring (BtB6) demonstrate insulin resistance in muscle tissue. Here, we report an insulin re

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Björnson Granqvist, Anna, Anette Ericsson, José Sanchez, et al. "High-protein diet accelerates diabetes and kidney disease in the BTBRob/ob mouse." American Journal of Physiology-Renal Physiology 318, no. 3 (2020): F763—F771. http://dx.doi.org/10.1152/ajprenal.00484.2019.

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There is a need for improved animal models that better translate to human kidney disease to predict outcome of pharmacological effects in the patient. The diabetic BTBR ob/ob mouse model mimics key features of early diabetic nephropathy in humans, but with chronic injury limited to glomeruli. To explore if we could induce an accelerated and more advanced disease phenotype that closer translates to human disease, we challenged BTBR ob/ob mice with a high-protein diet (HPD; 30%) and followed the progression of metabolic and renal changes up to 20 wk of age. Animals on the HPD showed enhanced met

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A., De Felice, Greco A., Calamandrei G., and Minghetti L. "Prenatal exposure to the organophosphate insecticide chlorpyrifos enhances brain oxidative stress and prostaglandin E2 synthesis in a mouse model of idiopathic autism." Journal of Neuroinflammation 13, no. 1 (2016): 149. https://doi.org/10.1186/s12974-016-0617-4.

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BACKGROUND: Autism spectrum disorders (ASD) are emerging as polygenic and multifactorial disorders in which complex interactions between defective genes and early exposure to environmental stressors impact on the correct neurodevelopment and brain processes. Organophosphate insecticides, among which chlorpyrifos (CPF), are widely diffused environmental toxicants associated with neurobehavioral deficits and increased risk of ASD occurrence in children. Oxidative stress and dysregulated immune responses are implicated in both organophosphate neurodevelopmental effects and ASD etiopathogenesis. B

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Assiri, Mohammed A., Thamer H. Albekairi, Mushtaq A. Ansari, et al. "The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR T+ Itpr3tf/J Mice through the Regulation of Signaling Pathways Relevant to T Cells." International Journal of Molecular Sciences 24, no. 22 (2023): 16218. http://dx.doi.org/10.3390/ijms242216218.

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Autism spectrum disorder (ASD) is a common neurodevelopmental illness characterized by abnormal social interactions, communication difficulties, and repetitive and limited behaviors or interests. The BTBR T+ Itpr3tf/J (BTBR) mice have been used extensively to research the ASD-like phenotype. Lead (Pb) is a hazardous chemical linked to organ damage in the human body. It is regarded as one of the most common metal exposure sources and has been connected to the development of neurological abnormalities. We used flow cytometry to investigate the molecular mechanism behind the effect of Pb exposure

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Li, Qi, Yaxin Shi, Xiang Li, et al. "Proteomic-Based Approach Reveals the Involvement of Apolipoprotein A-I in Related Phenotypes of Autism Spectrum Disorder in the BTBR Mouse Model." International Journal of Molecular Sciences 23, no. 23 (2022): 15290. http://dx.doi.org/10.3390/ijms232315290.

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder. Abnormal lipid metabolism has been suggested to contribute to its pathogenesis. Further exploration of its underlying biochemical mechanisms is needed. In a search for reliable biomarkers for the pathophysiology of ASD, hippocampal tissues from the ASD model BTBR T+ Itpr3tf/J (BTBR) mice and C57BL/6J mice were analyzed, using four-dimensional (4D) label-free proteomic analysis and bioinformatics analysis. Differentially expressed proteins were significantly enriched in lipid metabolic pathways. Among them, apolipoprotein A-I (Apo

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Ahn, Younghee, Rasha Sabouny, Bianca R. Villa, et al. "Aberrant Mitochondrial Morphology and Function in the BTBR Mouse Model of Autism Is Improved by Two Weeks of Ketogenic Diet." International Journal of Molecular Sciences 21, no. 9 (2020): 3266. http://dx.doi.org/10.3390/ijms21093266.

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Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder that exhibits a common set of behavioral and cognitive impairments. Although the etiology of ASD remains unclear, mitochondrial dysfunction has recently emerged as a possible causative factor underlying ASD. The ketogenic diet (KD) is a high-fat, low-carbohydrate diet that augments mitochondrial function, and has been shown to reduce autistic behaviors in both humans and in rodent models of ASD. The aim of the current study was to examine mitochondrial bioenergetics in the BTBR mouse model of ASD and to determine

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Algahtani, Mohammad M., Sheikh F. Ahmad, Layla A. Alkharashi, et al. "Exposure to Methylmercury at Juvenile Stage Worsens Autism-like Symptoms in Adult BTBR T+tf/J Mice Due to Lack of Nuclear Factor Erythroid 2-Related Factor 2 Signaling Upregulation in Periphery and Brain." Toxics 11, no. 6 (2023): 546. http://dx.doi.org/10.3390/toxics11060546.

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Autism spectrum disorder (ASD) is a multifaceted developmental condition that first appears in infancy. The condition is characterized by recurrent patterns in behavior and impairments in social and vocalization abilities. Methylmercury is a toxic environmental pollutant, and its derivatives are the major source of organic mercury to human beings. Inorganic mercury, which is released from a variety of pollutants into oceans, rivers, and streams, is transformed into methylmercury by bacteria and plankton in the water, which later builds up in fish and shellfish, and then enters humans through t

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Dørflinger, Gry H., Charlotte B. Holt, Steffen Thiel, Jesper N. Bech, Jakob A. Østergaard, and Mette Bjerre. "Mannan-Binding Lectin Is Associated with Inflammation and Kidney Damage in a Mouse Model of Type 2 Diabetes." International Journal of Molecular Sciences 25, no. 13 (2024): 7204. http://dx.doi.org/10.3390/ijms25137204.

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Autoreactivity of the complement system may escalate the development of diabetic nephropathy. We used the BTBR OB mouse model of type 2 diabetes to investigate the role of the complement factor mannan-binding lectin (MBL) in diabetic nephropathy. Female BTBR OB mice (n = 30) and BTBR non-diabetic WT mice (n = 30) were included. Plasma samples (weeks 12 and 21) and urine samples (week 19) were analyzed for MBL, C3, C3-fragments, SAA3, and markers for renal function. Renal tissue sections were analyzed for fibrosis, inflammation, and complement deposition. The renal cortex was analyzed for gene

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Eissa, Nermin, Mohamed Al Awad, Shilu Deepa Thomas, et al. "Simultaneous Antagonism at H3R/D2R/D3R Reduces Autism-like Self-Grooming and Aggressive Behaviors by Mitigating MAPK Activation in Mice." International Journal of Molecular Sciences 24, no. 1 (2022): 526. http://dx.doi.org/10.3390/ijms24010526.

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Dysregulation in brain neurotransmitters underlies several neuropsychiatric disorders, e.g., autism spectrum disorder (ASD). Also, abnormalities in the extracellular-signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) pathway pave the way for neuroinflammation, neurodegeneration, and altered learning phenotype in ASD. Therefore, the effects of chronic systemic administration of the multiple-targeting antagonist ST-713 at the histamine H3 receptor (H3R) and dopamine D2/D3 receptors (D2/D3R) on repetitive self-grooming, aggressive behaviors, and abnormalities in the MAPK pathwa

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Alshamrani, Ali A., Mohammad Y. Alwetaid, Mohammed A. Al-Hamamah, et al. "Aflatoxin B1 Exacerbates Genomic Instability and Apoptosis in the BTBR Autism Mouse Model via Dysregulating DNA Repair Pathway." Toxics 11, no. 7 (2023): 636. http://dx.doi.org/10.3390/toxics11070636.

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The pathophysiology of autism is influenced by a combination of environmental and genetic factors. Furthermore, individuals with autism appear to be at a higher risk of developing cancer. However, this is not fully understood. Aflatoxin B1 (AFB1) is a potent food pollutant carcinogen. The effects of AFB1 on genomic instability in autism have not yet been investigated. Hence, we have aimed to investigate whether repeated exposure to AFB1 causes alterations in genomic stability, a hallmark of cancer and apoptosis in the BTBR autism mouse model. The data revealed increased micronuclei generation,

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Cristiano, Claudia, Floriana Volpicelli, Marianna Crispino, et al. "Behavioral, Anti-Inflammatory, and Neuroprotective Effects of a Novel FPR2 Agonist in Two Mouse Models of Autism." Pharmaceuticals 15, no. 2 (2022): 161. http://dx.doi.org/10.3390/ph15020161.

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Autism spectrum disorders (ASD) are a group of heterogeneous neurodevelopmental conditions characterized by social deficits, repetitive stereotyped behaviors, and altered inflammatory responses. Accordingly, children with ASD show decreased plasma levels of lipoxin A4 (LXA4), a mediator involved in the resolution of inflammation, which is the endogenous ligand of the formyl peptide receptor 2 (FPR2). To investigate the role of FPR2 in ASDs, we have used a new ureidopropanamide derivative able to activate the receptor, named MR-39. The effects of MR-39 (10 mg/kg, for 8 days) on hippocampal pro-

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Karunakaran, Subashini, Akiff Manji, Chenhua Serena Yan, Zi-Jun John Wu, and Susanne M. Clee. "Moo1 obesity quantitative trait locus in BTBR T+ Itpr3tf/J mice increases food intake." Physiological Genomics 45, no. 5 (2013): F191—F199. http://dx.doi.org/10.1152/physiolgenomics.00159.2012.

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The rising prevalence of obesity is one of the greatest health challenges facing the world today. Discovery of genetic factors affecting obesity risk will provide important insight to its etiology that could suggest new therapeutic approaches. We have previously identified the Modifier of obese 1 ( Moo1) quantitative trait locus (QTL) in a cross between leptin-deficient BTBR T+ Itpr3tf/J (BTBR) and C57BL/6J (B6) mice. Understanding the mechanism by which this locus acts will aid in the identification of candidate genes. Here we refined the location of this QTL and sought to determine the mecha

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Thomas, Shilu Deepa, Petrilla Jayaprakash, Nurfirzana Z. H. J. Marwan, et al. "Alleviation of Autophagic Deficits and Neuroinflammation by Histamine H3 Receptor Antagonist E159 Ameliorates Autism-Related Behaviors in BTBR Mice." Pharmaceuticals 17, no. 10 (2024): 1293. http://dx.doi.org/10.3390/ph17101293.

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Background/Objectives: Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by social interaction difficulties, repetitive behaviors, and immune dysregulation with elevated pro-inflammatory markers. Autophagic deficiency also contributes to social behavior deficits in ASD. Histamine H3 receptor (H3R) antagonism is a potential treatment strategy for brain disorders with features overlapping ASD, such as schizophrenia and Alzheimer’s disease. Methods: This study investigated the effects of sub-chronic systemic treatment with the H3R antagonist E159 on social deficits, repetiti

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Squillace, M., L. Dodero, M. Federici, et al. "Dysfunctional dopaminergic neurotransmission in asocial BTBR mice." Translational Psychiatry 4, no. 8 (2014): e427-e427. http://dx.doi.org/10.1038/tp.2014.69.

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Bonetti, Matteo, Lorena Giugno, Elisa Borsani, and Francesca Bonomini. "Potential Neuroprotective Effect of Melatonin in the Hippocampus of Male BTBR Mice." Nutrients 16, no. 11 (2024): 1652. http://dx.doi.org/10.3390/nu16111652.

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder identified by impairments in common social interactions and repetitive behaviors. In ASD patients, substantial morphological alterations have been observed in the hippocampus, which represents an important region for the development of social skills. Melatonin, commonly found in many foods and plants, is also produced by the pineal gland. This indolamine, known to regulate the circadian rhythm, shows antioxidant and anti-inflammatory properties. We therefore hypothesized that melatonin may reduce oxidative stress and inflammation

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Alanazi, Mohammed M., Mushtaq A. Ansari, Ahmed Nadeem, et al. "Cadmium Exposure Is Associated with Behavioral Deficits and Neuroimmune Dysfunction in BTBR T+ Itpr3tf/J Mice." International Journal of Molecular Sciences 24, no. 7 (2023): 6575. http://dx.doi.org/10.3390/ijms24076575.

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Autism spectrum disorders (ASD) are neurobehavioral disabilities characterized by impaired social interactions, poor communication skills, and restrictive/repetitive behaviors. Cadmium is a common heavy metal implicated in ASD. In this study, we investigated the effects of Cd exposure on BTBR T+ Itpr3tf/J (BTBR) mice, an ASD model. We looked for changes in repetitive behaviors and sociability through experiments. We also explored the molecular mechanisms underlying the effects of Cd exposure, focusing on proinflammatory cytokines and pathways. Flow cytometry measured IL-17A-, IL-17F-, IL-21-,

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Sugahara, Mai, Shinji Tanaka, Tetsuhiro Tanaka, et al. "Prolyl Hydroxylase Domain Inhibitor Protects against Metabolic Disorders and Associated Kidney Disease in Obese Type 2 Diabetic Mice." Journal of the American Society of Nephrology 31, no. 3 (2020): 560–77. http://dx.doi.org/10.1681/asn.2019060582.

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BackgroundProlyl hydroxylase domain (PHD) inhibitors, which stimulate erythropoietin production through the activation of hypoxia-inducible factor (HIF), are novel therapeutic agents used for treating renal anemia. Several PHD inhibitors, including enarodustat, are currently undergoing phase 2 or phase 3 clinical trials. Because HIF regulates a broad spectrum of genes, PHD inhibitors are expected to have other effects in addition to erythropoiesis, such as protection against metabolic disorders. However, whether such beneficial effects would extend to metabolic disorder–related kidney disease

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Franco, Caterina, Francesca Bonomini, Elisa Borsani, Stefania Castrezzati, Lorenzo Franceschetti, and Rita Rezzani. "Involvement of Intestinal Goblet Cells and Changes in Sodium Glucose Transporters Expression: Possible Therapeutic Targets in Autistic BTBR T+Itpr3tf/J Mice." International Journal of Environmental Research and Public Health 18, no. 21 (2021): 11328. http://dx.doi.org/10.3390/ijerph182111328.

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Autism spectrum disorder is a neurodevelopmental syndrome with a complicated etiology and could be responsible for disrupted gastrointestinal tract microbiota. The aim of this work was to study intestinal samples from an autistic animal model (BTBR mouse strain) to better describe gastrointestinal alterations. We performed a morphological and biological evaluation of small intestine samples. In terms of morphology, we studied the goblet cells, cells of intestinal mucosal responsible for the production and maintenance of the protective mucous blanket. Alterations in their secretion may indicate

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Eissa, Nermin, Karthikkumar Venkatachalam, Petrilla Jayaprakash, et al. "Experimental Studies Indicate That ST-2223, the Antagonist of Histamine H3 and Dopamine D2/D3 Receptors, Restores Social Deficits and Neurotransmission Dysregulation in Mouse Model of Autism." Pharmaceuticals 15, no. 8 (2022): 929. http://dx.doi.org/10.3390/ph15080929.

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Altered regulation of neurotransmitters may lead to many pathophysiological changes in brain disorders including autism spectrum disorder (ASD). Given the fact that there are no FDA-approved effective treatments for the social deficits in ASD, the present study determined the effects of chronic systemic treatment of the novel multiple-active H3R/D2R/D3R receptor antagonist ST-2223 on ASD-related social deficits in a male Black and Tan Brachyury (BTBR) mice. ST-2223 (2.5, 5, and 10 mg/kg, i.p.) significantly and dose-dependently mitigated social deficits and disturbed anxiety levels of BTBR mic

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Eissa, Nermin, Karthikkumar Venkatachalam, Petrilla Jayaprakash, et al. "The Multi-Targeting Ligand ST-2223 with Histamine H3 Receptor and Dopamine D2/D3 Receptor Antagonist Properties Mitigates Autism-Like Repetitive Behaviors and Brain Oxidative Stress in Mice." International Journal of Molecular Sciences 22, no. 4 (2021): 1947. http://dx.doi.org/10.3390/ijms22041947.

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Autism spectrum disorder (ASD) is a complex heterogeneous neurodevelopmental disorder characterized by social and communicative impairments, as well as repetitive and restricted behaviors (RRBs). With the limited effectiveness of current pharmacotherapies in treating repetitive behaviors, the present study determined the effects of acute systemic treatment of the novel multi-targeting ligand ST-2223, with incorporated histamine H3 receptor (H3R) and dopamine D2/D3 receptor affinity properties, on ASD-related RRBs in a male Black and Tan BRachyury (BTBR) mouse model of ASD. ST-2223 (2.5, 5, and

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Alwetaid, Mohammad Y., Taghreed N. Almanaa, Saleh A. Bakheet, et al. "Aflatoxin B1 Exposure Aggravates Neurobehavioral Deficits and Immune Dysfunctions of Th1, Th9, Th17, Th22, and T Regulatory Cell-Related Transcription Factor Signaling in the BTBR T+Itpr3tf/J Mouse Model of Autism." Brain Sciences 13, no. 11 (2023): 1519. http://dx.doi.org/10.3390/brainsci13111519.

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Autism spectrum disorder (ASD) is a neurodevelopmental disease characterized by impaired communication, reciprocal social interactions, restricted sociability deficits, and stereotyped behavioral patterns. Environmental factors and genetic susceptibility have been implicated in an increased risk of ASD. Aflatoxin B1 (AFB1) is a typical contaminant of food and feed that causes severe immune dysfunction in humans and animals. Nevertheless, the impact of ASD on behavioral and immunological responses has not been thoroughly examined. To investigate this phenomenon, we subjected BTBR T+Itpr3tf/J (B

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Dong, Ziyi. "The effect of DNA polymeraseon autism tasted by aflatoxin B1." Theoretical and Natural Science 44, no. 1 (2024): 150–55. http://dx.doi.org/10.54254/2753-8818/44/20240830.

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Purpose: Since aflatoxins B1 can cause autism in mice by disrupting DNA repair and altering the stability of the genome, the study aims to see whether DNA pol alleviate autism tasted by AFB1, because of its DNA repair function. Whats more, the study would identify whether aflatoxins gene damage can be repaired by DNA polymerase . Methods: In this study, four groups of BTBR mice were selected. The positive group was normal BTBR mice, the other group was AFB1-infected mice, and the experimental group was AFB1-infected mice treated with DNA polymerase , the negative group was AFB1-infected mice w

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Pochakom, Angela, Chunlong Mu, Jong M. Rho, Thomas A. Tompkins, Shyamchand Mayengbam, and Jane Shearer. "Selective Probiotic Treatment Positively Modulates the Microbiota–Gut–Brain Axis in the BTBR Mouse Model of Autism." Brain Sciences 12, no. 6 (2022): 781. http://dx.doi.org/10.3390/brainsci12060781.

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Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed the impact of two probiotic strains in mitigating autism-related symptomology in the BTBR T+ Itpr3tf/J mouse model of autism spectrum disorder (ASD). Male juvenile BTBR mice were randomized into: (1) control, (2) Lr probiotic (1 × 109 CFU/mL Lacticaseibacillus rhamnosus HA-114), and (3) Ls probiotic groups (1 × 109 CFU/mL Ligilactobacillus salivarius HA-118) (n = 18–21/group), receiving treatments in drinking water for 4 weeks. Gut microbi

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Locatelli, Monica, Daniela Rottoli, Rayan Mahmoud, et al. "Endothelial Glycocalyx of Peritubular Capillaries in Experimental Diabetic Nephropathy: A Target of ACE Inhibitor-Induced Kidney Microvascular Protection." International Journal of Molecular Sciences 24, no. 22 (2023): 16543. http://dx.doi.org/10.3390/ijms242216543.

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Peritubular capillary rarefaction is a recurrent aspect of progressive nephropathies. We previously found that peritubular capillary density was reduced in BTBR ob/ob mice with type 2 diabetic nephropathy. In this model, we searched for abnormalities in the ultrastructure of peritubular capillaries, with a specific focus on the endothelial glycocalyx, and evaluated the impact of treatment with an angiotensin-converting enzyme inhibitor (ACEi). Mice were intracardially perfused with lanthanum to visualise the glycocalyx. Transmission electron microscopy analysis revealed endothelial cell abnorm

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Jayaprakash, Petrilla, Dmytro Isaev, Keun-Hang Susan Yang, Rami Beiram, Murat Oz, and Bassem Sadek. "Apigenin Alleviates Autistic-like Stereotyped Repetitive Behaviors and Mitigates Brain Oxidative Stress in Mice." Pharmaceuticals 17, no. 4 (2024): 482. http://dx.doi.org/10.3390/ph17040482.

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Studying the involvement of nicotinic acetylcholine receptors (nAChRs), specifically α7-nAChRs, in neuropsychiatric brain disorders such as autism spectrum disorder (ASD) has gained a growing interest. The flavonoid apigenin (APG) has been confirmed in its pharmacological action as a positive allosteric modulator of α7-nAChRs. However, there is no research describing the pharmacological potential of APG in ASD. The aim of this study was to evaluate the effects of the subchronic systemic treatment of APG (10–30 mg/kg) on ASD-like repetitive and compulsive-like behaviors and oxidative stress sta

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Hudkins, Kelly L., Tomasz A. Wietecha, Floor Steegh, and Charles E. Alpers. "Beneficial effect on podocyte number in experimental diabetic nephropathy resulting from combined atrasentan and RAAS inhibition therapy." American Journal of Physiology-Renal Physiology 318, no. 5 (2020): F1295—F1305. http://dx.doi.org/10.1152/ajprenal.00498.2019.

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Podocyte loss and proteinuria are both key features of human diabetic nephropathy (DN). The leptin-deficient BTBR mouse strain with the ob/ob mutation develops progressive weight gain, type 2 diabetes, and diabetic nephropathy that has many features of advanced human DN, including increased mesangial matrix, mesangiolysis, podocyte loss, and proteinuria. Selective antagonism of the endothelin-1 type A receptor (ETAR) by atrasentan treatment in combination with renin-angiotensin-aldosterone system inhibition with losartan has been shown to have the therapeutic benefit of lowering proteinuria in

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Rosendahl, Alexander, Maiken Pedersen, and Lisbeth Fink. "Imbalanced adoptive immunity in the diabetic nephropatic BTBR ob/ob mouse (IRC4P.474)." Journal of Immunology 192, no. 1_Supplement (2014): 60.1. http://dx.doi.org/10.4049/jimmunol.192.supp.60.1.

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Abstract Human diabetic nephropathy (DN) has extensive kidney fibrosis and inflammation. The BTBRob/ob mouse model has kidney fibrosis, but the inflammatory status is not known. Herein, we investigated the systemic and local lymphocytic immunity in the BTBRob/ob mouse. The BTBRob/ob mouse developed hyperglycaemia and albuminuria. The diabetic kidney had similar numbers of CD4+, enhanced CD8+ T cells and reduced B cells as the ob+ control. The BTBR ob/ob had moderately enhanced spleen size without significant modulation of the T or B cells numbers. Interestingly, the BTBRob/ob CD4 cells had an

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Hudkins, Kelly L., Warangkana Pichaiwong, Tomasz Wietecha, et al. "BTBR Ob/Ob Mutant Mice Model Progressive Diabetic Nephropathy." Journal of the American Society of Nephrology 21, no. 9 (2010): 1533–42. http://dx.doi.org/10.1681/asn.2009121290.

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Vijaya Shankara, Jhenkruthi, Katelyn G. Horsley, Naila F. Jamani, Zhi A. Robinson, Joanne R. Y. Kwong, and Michael C. Antle. "Circadian responses to non-photic treatments in BTBR mice." Physiology & Behavior 297 (August 2025): 114947. https://doi.org/10.1016/j.physbeh.2025.114947.

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