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Relevant bibliographies by topics / Novel diet-induced mice model

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Academic literature on the topic 'Novel diet-induced mice model'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "Novel diet-induced mice model"

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Ichimura-Shimizu, Mayuko, Katsuhisa Omagari, Michiko Yamashita, and Koichi Tsuneyama. "Development of a novel mouse model of diet-induced nonalcoholic steatohepatitis–related progressive bridging fibrosis." Bioscience, Biotechnology, and Biochemistry 85, no. 4 (2020): 941–47. http://dx.doi.org/10.1093/bbb/zbaa107.

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ABSTRACT Nonalcoholic steatohepatitis (NASH) progresses to liver fibrosis and cirrhosis. Existing mouse models of NASH rarely develop diet-induced severe fibrosis. We aimed to establish a dietary model of NASH with rapid progression to fibrosis. Six-week-old male Tsumura-Suzuki obese diabetes (TSOD) mice (a model of spontaneous metabolic syndrome) and corresponding control Tsumura-Suzuki nonobese (TSNO) mice were fed a novel diet high in fat, cholesterol, and cholate (iHFC). Histologic steatohepatitis, including steatosis, inflammation, and fibrosis, were observed in both TSNO and TSOD iHFC di

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Halperin Kuhns, Victoria L., and Jennifer L. Pluznick. "Novel differences in renal gene expression in a diet-induced obesity model." American Journal of Physiology-Renal Physiology 314, no. 4 (2018): F517—F530. http://dx.doi.org/10.1152/ajprenal.00345.2017.

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Obesity is a significant risk factor for both chronic kidney disease and end-stage renal disease. To better understand disease development, we sought to identify novel genes differentially expressed early in disease progression. We first confirmed that mice fed a high-fat (HF) diet exhibit early signs of renal injury including hyperfiltration. We then performed RNA-Seq using renal cortex RNA from C57BL6/J male mice fed either HF or control (Ctrl) diet. We identified 1,134 genes differentially expressed in the cortex on HF vs. Ctrl, of which 31 genes were selected for follow-up analysis. This i

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Zuloaga, Kristen L., Lance A. Johnson, Natalie E. Roese, et al. "High fat diet-induced diabetes in mice exacerbates cognitive deficit due to chronic hypoperfusion." Journal of Cerebral Blood Flow & Metabolism 36, no. 7 (2015): 1257–70. http://dx.doi.org/10.1177/0271678x15616400.

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Diabetes causes endothelial dysfunction and increases the risk of vascular cognitive impairment. However, it is unknown whether diabetes causes cognitive impairment due to reductions in cerebral blood flow or through independent effects on neuronal function and cognition. We addressed this using right unilateral common carotid artery occlusion to model vascular cognitive impairment and long-term high-fat diet to model type 2 diabetes in mice. Cognition was assessed using novel object recognition task, Morris water maze, and contextual and cued fear conditioning. Cerebral blood flow was assesse

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Weerasekera, Lakshini, Caroline Rudnicka, Qing-Xiang Sang, et al. "ADAM19: A Novel Target for Metabolic Syndrome in Humans and Mice." Mediators of Inflammation 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7281986.

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Obesity is one of the most prevalent metabolic diseases in the Western world and correlates directly with insulin resistance, which may ultimately culminate in type 2 diabetes (T2D). We sought to ascertain whether the human metalloproteinase A Disintegrin and Metalloproteinase 19 (ADAM19) correlates with parameters of the metabolic syndrome in humans and mice. To determine the potential novel role of ADAM19 in the metabolic syndrome, we first conducted microarray studies on peripheral blood mononuclear cells from a well-characterised human cohort. Secondly, we examined the expression of ADAM19

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Cui, Wenpeng, Yangwei Wang, Qiang Chen, et al. "MagnoliaExtract (BL153) Ameliorates Kidney Damage in a High Fat Diet-Induced Obesity Mouse Model." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/367040.

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Accumulating evidence demonstrated that obesity is a risk factor for renal structural and functional changes, leading to the end-stage renal disease which imposes a heavy economic burden on the community. However, no effective therapeutic method for obesity-associated kidney disease is available. In the present study, we explored the therapeutic potential of amagnoliaextract (BL153) for treating obesity-associated kidney damage in a high fat diet- (HFD-) induced mouse model. The results showed that inflammation markers (tumor necrosis factor-αand plasminogen activator inhibitor-1) and oxidativ

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Meggyesy, Peter M., Shashank Masaldan, Sharnel A. S. Clatworthy, et al. "Copper Ionophores as Novel Antiobesity Therapeutics." Molecules 25, no. 21 (2020): 4957. http://dx.doi.org/10.3390/molecules25214957.

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The therapeutic utility of the copper ionophore disulfiram was investigated in a diet-induced obesity mouse model (C57BL/6J background), both through administration in feed (0.05 to 1% (w/w)) and via oral gavage (150 mg/kg) for up to eight weeks. Mice were monitored for body weight, fat deposition (perigonadal fat pads), metabolic changes (e.g., glucose dyshomeostasis) and pathologies (e.g., hepatic steatosis, hyperglycaemia and hypertriglyceridemia) associated with a high-fat diet. Metal-related pharmacological effects across major organs and serums were investigated using inductively coupled

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Malhotra, Pooja, Costica Aloman, Aparna Ankireddy, et al. "Overactivation of intestinal sterol response element-binding protein 2 promotes diet-induced nonalcoholic steatohepatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 5 (2017): G376—G385. http://dx.doi.org/10.1152/ajpgi.00174.2017.

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Nonalcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation in the liver that may progress to hepatic fibrosis and nonalcoholic steatohepatitis (NASH). Mechanisms underlying NAFLD and NASH are not yet fully understood. Dietary cholesterol was recently shown to be a risk factor for the development of NASH, suggesting a role for intestinal handling of cholesterol. One important regulator of cholesterol homeostasis is the sterol response element-binding protein-2 (SREBP-2) transcription factor. We tested the hypothesis that the overactivation of intestinal SREBP-2 increases th

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Lee, Katie T. Y., Subashini Karunakaran, Maggie M. Ho, and Susanne M. Clee. "PWD/PhJ and WSB/EiJ Mice Are Resistant to Diet-Induced Obesity But Have Abnormal Insulin Secretion." Endocrinology 152, no. 8 (2011): 3005–17. http://dx.doi.org/10.1210/en.2011-0060.

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Recently, novel inbred mouse strains that are genetically distinct from the commonly used models have been developed from wild-caught mice. These wild-derived inbred strains have been included in many of the large-scale genomic projects, but their potential as models of altered obesity and diabetes susceptibility has not been assessed. We examined obesity and diabetes-related traits in response to high-fat feeding in two of these strains, PWD/PhJ (PWD) and WSB/EiJ (WSB), in comparison with C57BL/6J (B6). Young PWD mice displayed high fasting insulin levels, although they had normal insulin sen

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Pouwer, Marianne G., Suvi E. Heinonen, Margareta Behrendt, et al. "The APOE∗3-Leiden Heterozygous Glucokinase Knockout Mouse as Novel Translational Disease Model for Type 2 Diabetes, Dyslipidemia, and Diabetic Atherosclerosis." Journal of Diabetes Research 2019 (February 21, 2019): 1–13. http://dx.doi.org/10.1155/2019/9727952.

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Background. There is a lack of predictive preclinical animal models combining atherosclerosis and type 2 diabetes. APOE∗3-Leiden (E3L) mice are a well-established model for diet-induced hyperlipidemia and atherosclerosis, and glucokinase+/− (GK+/−) mice are a translatable disease model for glucose control in type 2 diabetes. The respective mice respond similarly to lipid-lowering and antidiabetic drugs as humans. The objective of this study was to evaluate/characterize the APOE∗3-Leiden.glucokinase+/− (E3L.GK+/−) mouse as a novel disease model to study the metabolic syndrome and diabetic compl

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Peterson, Jonathan M., Marcus M. Seldin, Zhikui Wei, Susan Aja, and G. William Wong. "CTRP3 attenuates diet-induced hepatic steatosis by regulating triglyceride metabolism." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 3 (2013): G214—G224. http://dx.doi.org/10.1152/ajpgi.00102.2013.

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CTRP3 is a secreted plasma protein of the C1q family that helps regulate hepatic gluconeogenesis and is downregulated in a diet-induced obese state. However, the role of CTRP3 in regulating lipid metabolism has not been established. Here, we used a transgenic mouse model to address the potential function of CTRP3 in ameliorating high-fat diet-induced metabolic stress. Both transgenic and wild-type mice fed a high-fat diet showed similar body weight gain, food intake, and energy expenditure. Despite similar adiposity to wild-type mice upon diet-induced obesity (DIO), CTRP3 transgenic mice were

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Dissertations / Theses on the topic "Novel diet-induced mice model"

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Kürten, Stephanie. "MP4-induced experimental autoimmune encephalomyelitis in C57BL/6 mice as a novel model for multiple sclerosis and its treatment /." Köln, 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000278345.

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Guedes, Glaucevane da Silva. "Estudo hepático de um modelo murino dietético para síndrome metabólica: perfil morfológico, funcional e balanço redox." Universidade Federal de Alagoas, 2009. http://repositorio.ufal.br/handle/riufal/635.

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Changes in lifestyle of people has been dynamically observed in recent decades, emphasis is given to dietary issues. In this case, as directly responsible for chronic diseases, along with other aspects of lifestyle such as inactivity, smoking, quality of life. In the context of chronic diseases of high incidence and prevalence, the metabolic syndrome has gained prominence in clinical and experimental research in the search for early diagnostic methods for its various components such as the vascular, biochemical and liver, all also associated with diet. In this context, there was the inclusion

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Eastgard, Rebecca Lugar. "Diet-induced hyperhomocysteinemia in a mouse model /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6601.

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Thomas, Amandine. "Hypoxie intermittente et homéostasie glucidique : étude des mécanismes d'action cellulaire A hybrid model to study pathological mutations of the human ADP/ATP carriers Visceral white fat remodeling contributes to intermittent hypoxia-induced atherogenesis The insulin sensitizing effect of topiramate involves KATP channel activation in the central nervous system The Impact of Sleep Disorders on Glucose Metabolism: Endocrine and Molecular Mechanisms Endoplasmic reticulum stress as a novel inducer of hypoxia inducible factor-1 activity: its role in the susceptibility to myocardial ischemia-reperfusion induced by chronic intermittent hypoxia Chronic intermittent hypoxia improves whole-body glucose tolerance by activating skeletal muscle AMP-activated protein kinase in mice Prolyl-4-hydroxylase 1 (PHD1) deficiency impairs whole-body glucose tolerance and insulin sensitivity in mice but does not worsen high-fat diet-induced metabolic dysfunctions Specific transcriptomic signature in response to intermittent hypoxia exposure in liver and fat tissue." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAV044.

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L'hypoxie intermittente (HI), induite par les apnées du sommeil, conduit à des altérations de la sensibilité à l'insuline et de l'homéostasie glucidique mais les mécanismes impliqués restent mal connus. L'objectif de ce travail était d'étudier les effets et les mécanismes sous jacents d'une exposition chronique à l'HI sur l'homéostasie glucidique. L'HI induit une résistance à l'insuline à la fois systémique et tissulaire, ainsi qu'une amélioration de la tolérance au glucose associée à une activation de l'AMPK musculaire. L'HI cause également des altérations du foie et du tissu adipeux associée

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Ludwig, Tobias [Verfasser], B. L. [Akademischer Betreuer] Bader, Johann J. [Akademischer Betreuer] Hauner, Hannelore [Akademischer Betreuer] Daniel, and ! [Mitwirkender]. "Novel effects of n-3 LC-PUFA on adipose tissue and liver in diet-induced obesity in mice / Tobias Ludwig. Gutachter: Hannelore Daniel. Betreuer: B. L. Bader ; Johann J. Hauner." München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/1024964183/34.

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Abdesselam, Inès. "Dépôts de graisse ectopique : étude de leur développement et de leur modulation." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5005.

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Le projet de cette thèse porte sur le développement de dépôts lipidiques ectopique et leur modulation suite à des intervenions thérapeutiques par imagerie résonance magnétique.Dans notre première étude, nous avons établi l’ordre chronologique d’apparition de graisses ectopiques et d’anomalies cardiaques dans un modèle de souris soumises à un régime riche en graisse et en sucre. Un traitement de courte durée à l’exendine-4 permet une amélioration de tous les paramètres altérés. Dans la deuxième étude, nous avons évalué l’impact d’un traitement de l’obésité sur les dépôts ectopique de graisse ca

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Kuo, Wen-Chun, and 郭玟君. "The novel neuroprotective effects and mechanism of lactic acid bacteria YM_A in MPTP-induced Parkinson's disease-like mice model." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/06964567610387600273.

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Ni, Yen-Hsiu, and 倪彥綉. "Effect of novel pigeon pea milk on high fat diet induced hepatic lipid accumulation in mice." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/362ds8.

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碩士<br>國立嘉義大學<br>食品科學系研究所<br>106<br>Cajanus cajan Linn. Millsp. is Leguminosae, Cajanus, and pigeon pea. It is one of the most important traditional food crops of Taiwanese aborigines. In recent years, there have been soybean milk products based on different beans, such as black soybean milk, soybean milk, and red soybean milk. Cajanus cajan L.of NO. 3 has been demonstrated to possess numerous biological effects such as antioxidant, anti-bacterial, anti-tumor, anti-viral and glycemic control. The present study aimed to investigate the pigeon pea milk (PPM) was made from Cajanus cajan L.of NO. 3

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Jie-KuanLin and 林玠寬. "Role of KATP channel in dopaminergic transmission using high fat diet-induced depression mice model." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/n99k7x.

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Basciano, Heather. "Development and characterization of a novel animal model of diet-induced insulin resistant diabetes and metabolic dyslipidemia: Mechanistic interactions between dietary fructose, fat and cholesterol, and the possible role of liver X receptor in the induction of metabolic syndrome." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=442072&T=F.

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Books on the topic "Novel diet-induced mice model"

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Basciano, Heather. Development and characterization of a novel animal model of diet-induced insulin resistant diabetes and metabolic dyslipidemia: Mechanistic interactions between dietary fructose, fat and cholesterol, and the possible role of liver X receptor in the induction of metabolic syndrome. 2006.

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Klepper, Joerg. Glut1 Deficiency and the Ketogenic Diets. Edited by Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0005.

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Glucose is the essential fuel for the brain. Transport into brain is exclusively mediated by the facilitative glucose transporter Glut1. Glut1 deficiency results in a “brain energy crisis,” causing global developmental delay, epilepsy, and complex movement disorders including paroxysmal nonepileptic events. Early-onset absence epilepsy, paroxysmal exertion-induced dystonia, and stomatin-deficient cryohydrocytosis have been recognized as variants. Diagnosis is based on phenotype, isolated low CSF glucose, and mutations in the SLC2A1 gene. The condition is treated effectively by classical ketoge

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Book chapters on the topic "Novel diet-induced mice model"

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Perez-Tilve, D., M. Tao, N. Ottaway, et al. "A Novel GLP-1/GIP Dual Agonist Normalizes Glucose Tolerance and Fat Mass in Diet Induced Obese Mice." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part2.p11.p2-511.

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Wang, Cecilia C. Low, Ya Xu, J. Wayne Leitner, et al. "Blunted Vascular Pi3-Kinase Signaling in a Novel Porcine Model of Diet-Induced Obesity Is Due to Increased Total P85alpha and Is Accompanied by Vascular Dysfunction." In BASIC/TRANSLATIONAL - Diet, Nutrients & Obesity: Impact on Inflammation & Adipose Tissue. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p33.p3-377.

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Conference papers on the topic "Novel diet-induced mice model"

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Agouni, Abdelali, Duck Y. Lee, Assaad A. Eid, Yves Gorin, and Kumar Sharma. "The Protective Role of Sestrin2 in High Fat Diet-Induced Nephropathy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0134.

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Introduction: Obesity is a major risk factor for type-2 diabetes predisposing patients to diabetic nephropathy (DN), the leading cause of end-stage renal failure. Glomerular injury is a prominent pathological feature of DN. Sestrin2 (Sesn2) is a stress-induced protein, but its role in DN has not been investigated. Therefore, we have determined the impact of Sesn2 deletion in a mouse model of obesityinduced nephropathy. Materials and methods: We examined the effects of Sesn2-deficiency in a longterm (22 weeks) mouse model of high fat diet (HFD)-induced obesity on glomerular structure. The sever

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Takahashi, K., H. Sadamatsu, H. Tashiro, et al. "An Effect of Novel Non-Antibiotic Macrolide EM900 in HDM-Induced Airway Inflammation Mice Model." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2894.

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Hoi, Yiemeng, Mark Van Doormaal, Yu-Qing Zhou, Xiaoli Zhang, R. Mark Henkelman, and David A. Steinman. "Degree of Retrograde Flow and Its Effect on Local Hemodynamics and Plaque Distribution in an Aortic Regurgitation Murine Model of Atherosclerosis." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53161.

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Previously, Zhou et al. [1] presented a novel mouse model of aortic valve regurgitation (AR) to explore the effect of altered hemodynamics on atherogenesis. In these ldlr−/− mice with AR, extensive atherosclerotic plaque was found along the naturally lesion-free descending thoracic (DTAo) and abdominal aorta (AbAo), with distinct spatial distributions suggestive of a strong local hemodynamic influence (Fig. 1, top). Doppler ultrasound measurement showed that both DTAo and AbAo of the AR mice experienced an oscillatory flow pattern induced by the diastolic retrograde flow, as opposed to the con

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Van Doormaal, M. A., X. Zhang, Y. Zhou, D. A. Steinman, and R. M. Henkelman. "In Vivo MRI Versus Ex Vivo CT for Image-Based CFD of the Mouse Aorta." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80118.

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A novel mouse model of surgically induced aortic valve regurgitation (AR) has been developed which leads to altered hemodynamics in the descending thoracic and abdominal aorta, in turn leading to extensive atherosclerotic lesions in these otherwise lesion free areas [1]. Previous work has shown that maps of oscillatory shear index (OSI) and relative residence time (RRT) are consistent with the plaque distribution [2] and plaque severity in AR mice.

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Liu, Ping, Xiaomin Ren, and Lisa X. Xu. "Alternate Cooling and Heating Thermal Physical Treatment: An Effective Strategy Against MDSCs in 4T1 Mouse Mammary Carcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80229.

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An alternate thermal physical treatment was developed to destroy tumor tissue using liquid nitrogen cooling and RF heating treatment in our pervious study. Our pervious reports had shown that anti-tumor immunity was induced by the alternate treatment. Myeloid derived suppressor cells (MDSCs) are a subset of heterogeneous, bone marrow derived hematopoietic cells that accumulate in the spleen, bone marrow, blood and tumor sites of tumor-bearing mice and cancer patients. MDSCs are one of the key suppressor cells that regulate anti-tumor immune responses in tumor-bearing hosts. MDSCs have been sho

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Soofi, Abdul. "The Kielin/chordin-like Protein Kcp Can Attenuate High Fat Diet Induced Obesity And Metabolic Syndrome In Mice Model." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0200.

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Santucci, Leticia, Marcio Torsoni, Anelise de Souza, et al. "The hypothalamic inflammation on a mice model of sepsis induced by cecal ligation puncture (CLP) procedure after the consumption of a short-term high-fat diet." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192302.

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Ramos-Ramirez, Patricia, Malin Noreby, Jielu Liu, et al. "A novel house dust mite-induced asthma model in guinea pigs driven by mast cells." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5001.

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