Готові списки джерел за темами / BTBR mice

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Добірка наукової літератури з теми "BTBR mice"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 31 липня 2025

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Статті в журналах з теми "BTBR mice"

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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Більше джерел

Дисертації з теми "BTBR mice"

LIN, CHIEN-MING, and 林建銘. "Generation of KLHL3 BTB Domain Mutation Mice to Elucidate the Role of WNK4 Kinase on Pseudohypoaldosteronism Type II." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/5v3nh2.

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博士<br>國防醫學院<br>醫學科學研究所<br>107<br>As opposed to Gitelman syndrome (GS) caused by loss-of-function mutation in the Na+-Cl- cotransporter (NCC), pseudohypoaldosteronism type II (PHAII) is notable for an enhanced NCC function. PHAII is an autosomal dominant renal tubular disorder characterized by thiazide-correctable salt-sensitive hypertension with low renin activity, hyperkalemic metabolic acidosis and hypercalciuria. Despite no identified NCC mutation in PHAII, genetic defects in the well-known with-no-lysine [K] (WNK) kinases WNK1 and WNK4 (minority) and two newly-discovered Kelch-like 3 (KLHL

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Частини книг з теми "BTBR mice"

McCarty, Richard. "Stress and Autism Spectrum Disorder." In Stress and Mental Disorders: Insights from Animal Models. Oxford University Press, 2020. http://dx.doi.org/10.1093/med-psych/9780190697266.003.0009.

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Animal models of autism spectrum disorder (ASD) seek to capture three of the cardinal symptoms of the disorder in affected children: deficits in social interactions, deficits in communication, and repetitive behaviors. In addition, males are more likely to develop ASD than females. The complex and variable presentation of ASD appears to involve genetic, environmental, and epigenetic contributions. The inbred BTBR mouse strain has frequently been utilized as an animal model of ASD. Other animal models have included a variety of prenatal insults, including maternal immune activation or administr

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Тези доповідей конференцій з теми "BTBR mice"

Kolesnikova, M. M., K. A. Ayriyant, E. V. Mezhlumyan, and N. P. Bondar. "INFLUENCE OF EARLY POSTNATAL INFLAMMATION ON GLIAL CELLS AND HYPOTHALAMIC-PITITUITARY-ADRENAL AXIS IN BTBR MALES." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-244.

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BTBR T+Itpr3tf/J (BTBR) mice are a valid model for studying idiopathic autism. This work examines the ability of the experience of induced early postnatal inflammation to enhance neuroinflammation and aberrant functioning of the hypothalamic-pituitary-adrenal axis observed in both patients with autism and BTBR mice.

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Qiu, J., T. Albrecht, S. Zhang, BK Krämer, and B. Yard. "Human CN1 overexpression aggravates diabetes and renal impairment in BTBR ob/ob mice." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688335.

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"The role of BDNF in the mechanisms of autistic-like behavior in BTBR mice." In Биоинформатика регуляции и структуры геномов / системная биология. ИЦиГ СО РАН, 2024. http://dx.doi.org/10.18699/bgrs2024-7.3-17.

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"Influence of administration of pro-inflammatory agents on development, individual and social behavior of BTBR mice." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-543.

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"Effect of Cc2d1a gene reduction the expression in hippocampus on behavior of BTBR mice – the model of autistic-like behavior of mice." In Systems Biology and Bioinformatics (SBB-2021) : The 13th International Young Scientists School;. ICG SB RAS, 2021. http://dx.doi.org/10.18699/sbb-plantgen-2021-01.

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"Different immune challenges alter hypothalamic microglia and astrocytes activity in the adult BTBR and C57Bl/6 mice." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-413.

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"Influence of 5-HT1A receptors overexpression in the hippocampus on behavior and the brain serotonin system of BTBR mice – the model of autism." In SYSTEMS BIOLOGY AND BIOINFORMATICS (SBB-2020). Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences., 2020. http://dx.doi.org/10.18699/sbb-2020-04.

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