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

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

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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3

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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9

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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Lednovich, Kristen Roan, Sophie Gough, Medha Priyadarshini, and Brian T. Layden. "Loss of Intestine-Specific FFA3 Has Protective Effects Against Diet-Induced Obesity and Hyperglycemia in Mice on a Western Diet." Journal of the Endocrine Society 5, Supplement_1 (2021): A441. http://dx.doi.org/10.1210/jendso/bvab048.901.

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Abstract Free fatty acid receptor 3 (FFA3) is a recently-deorphaned G protein-coupled receptor belonging to the free fatty acid receptor family. Its ligands are short-chain fatty acids (SCFAs), which are key nutrients that play a diverse role in physiological function, including the regulation of metabolic homeostasis and glycemic control. FFA3 is broadly expressed in a multitude of tissues including the intestine, pancreas, and central nervous system, and is thought to contribute to metabolic homeostasis via a summation of its tissue-specific effects. Consequently, FFA3 has been identified as

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Duchesnes, Cécile E., Jürgen K. Naggert, Michele A. Tatnell, et al. "New Zealand Ginger mouse: novel model that associates the tyrp1b pigmentation gene locus with regulation of lean body mass." Physiological Genomics 37, no. 3 (2009): 164–74. http://dx.doi.org/10.1152/physiolgenomics.90336.2008.

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The study of spontaneous mutations in mice over the last century has been fundamental to our understanding of normal physiology and mechanisms of disease. Here we studied the phenotype and genotype of a novel mouse model we have called the New Zealand Ginger (NZG/Kgm) mouse. NZG/Kgm mice are very large, rapidly growing, ginger-colored mice with pink eyes. Breeding NZG/Kgm mice with CAST/Ei or C57BL/6J mice showed that the ginger coat colour is a recessive trait, while the excessive body weight and large body size exhibit a semidominant pattern of inheritance. Backcrossing F1 (NZG/Kgm × CAST/Ei

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Yang, Jinho, Andrea McDowell, Eun Kyoung Kim, et al. "Development of a colorectal cancer diagnostic model and dietary risk assessment through gut microbiome analysis." Experimental & Molecular Medicine 51, no. 10 (2019): 1–15. http://dx.doi.org/10.1038/s12276-019-0313-4.

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Abstract Colorectal cancer (CRC) is the third most common form of cancer and poses a critical public health threat due to the global spread of westernized diets high in meat, cholesterol, and fat. Although the link between diet and colorectal cancer has been well established, the mediating role of the gut microbiota remains elusive. In this study, we sought to elucidate the connection between the gut microbiota, diet, and CRC through metagenomic analysis of bacteria isolated from the stool of CRC (n = 89) and healthy (n = 161) subjects. This analysis yielded a dozen genera that were significan

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Reilly, Michael P., Scott K. Dessain, Scott M. Taylor, et al. "Dietary Hypercholesterolemia Enhances Heparin-Induced Thrombocytopenia/Thrombosis: A Prothrombotic Risk Factor in a Transgenic Mouse Model." Blood 106, no. 11 (2005): 56. http://dx.doi.org/10.1182/blood.v106.11.56.56.

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Abstract Heparin-induced thrombocytopenia/thrombosis (HIT/T), the most frequent drug-induced immune thrombocytopenia, is a common cause of life- and limb-threatening thrombosis. Although heparin/platelet factor 4 (PF4) antibodies are detected in many patients treated with heparin, there is little understanding of why only a subset of patients develops thrombosis. We recently produced and characterized the first mouse model that recapitulates the salient features of the disease. A second generation model, designated IIA/hPF4-mPF4KO, expresses human FcγRIIA and PF4 but lacks endogenous mouse PF4

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15

Clemmensen, Christoffer, Sanela Smajilovic, Andreas N. Madsen, Anders B. Klein, Birgitte Holst, and Hans Bräuner-Osborne. "Increased susceptibility to diet-induced obesity in GPRC6A receptor knockout mice." Journal of Endocrinology 217, no. 2 (2013): 151–60. http://dx.doi.org/10.1530/joe-12-0550.

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The recently identified G protein-coupled receptor GPRC6A is activated by dietary amino acids and expressed in multiple tissues. Although the receptor is hypothesised to exert biological impact on metabolic and endocrine-related parameters, the role of the receptor in obesity and metabolic complications is still elusive. In the present study, we investigated the impact of GPRC6A deficiency in a murine model of diet-induced obesity (DIO). MaleGprc6aknockout (KO) mice and WT littermates were subjected to a high-fat diet (HFD) for 25 weeks and exposed to comprehensive metabolic phenotyping. A sig

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16

Brol, Maximilian Joseph, Stella Georgiou, Ditlev Nytoft Rasmussen, et al. "Effects of Ethanol Feeding in Early-Stage NAFLD Mice Induced by Western Diet." Livers 1, no. 1 (2021): 27–39. http://dx.doi.org/10.3390/livers1010003.

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Background: The prevalence of metabolic liver diseases is increasing and approved pharmacological treatments are still missing. Many animal models of nonalcoholic fatty liver disease (NAFLD) show a full spectrum of fibrosis, inflammation and steatosis, which does not reflect the human situation since only up to one third of the patients develop fibrosis and nonalcoholic steatohepatitis (NASH). Methods: Seven week old C57Bl/J mice were treated with ethanol, Western diet (WD) or both. The animals’ liver phenotypes were determined through histology, immunohistochemistry, Western blotting, hepatic

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Chen, Geng, and Shuodong Wu. "Role of Baicalin and Liver X Receptor Alpha in the Formation of Cholesterol Gallstones in Mice." Gastroenterology Research and Practice 2020 (April 21, 2020): 1–13. http://dx.doi.org/10.1155/2020/1343969.

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This study was aimed at investigating the effect of baicalin on experimental cholesterol gallstones in mice. The mouse gallstone model was induced by feeding with a lithogenic diet, and cholesterol stones were found in the gallbladder. The lithogenic diet caused elevation of triglycerides, cholesterol, and low-density lipoprotein concentrations and descent of high-density lipoprotein concentration in serum. Hyperplasia and inflammatory infiltration were observed in the gallbladder wall of lithogenic diet-fed mice. We also found the increase of cholesterol content and the decrease of bile acid

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Watanabe, Junji, James A. Lin, Ajay J. Narasimha, et al. "Novel anti-inflammatory functions for endothelial and myeloid cyclooxygenase-2 in a new mouse model of Crohn's disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (2010): G842—G850. http://dx.doi.org/10.1152/ajpgi.00468.2009.

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Cyclooxygenase-2 (COX-2) is an important regulator of inflammation implicated in the development of a variety of diseases, including inflammatory bowel disease (IBD). However, the regulation of intestinal inflammation by COX-2 is poorly understood. We previously reported that COX-2−/− mice fed a cholate-containing high-fat (CCHF) diet had high mortality of unknown mechanisms attributable to severe intestinal inflammation in the ileo-ceco-colic junction that presented characteristics similar to Crohn's disease (CD). To further characterize the role of COX-2 in intestinal inflammation, we establ

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Tan, Stefanie Y., Hannah C. Little, Xia Lei, Shuoyang Li, Susana Rodriguez, and G. William Wong. "Partial deficiency of CTRP12 alters hepatic lipid metabolism." Physiological Genomics 48, no. 12 (2016): 936–49. http://dx.doi.org/10.1152/physiolgenomics.00111.2016.

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Secreted hormones play pivotal roles in tissue cross talk to maintain physiologic blood glucose and lipid levels. We previously showed that C1q/TNF-related protein 12 (CTRP12) is a novel secreted protein involved in regulating glucose metabolism whose circulating levels are reduced in obese and insulin-resistant mouse models. Its role in lipid metabolism, however, is unknown. Using a novel heterozygous mouse model, we show that the loss of a single copy of the Ctrp12 gene (also known as Fam132a and adipolin) affects whole body lipid metabolism. In Ctrp12 (+/−) male mice fed a control low-fat d

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Pirman, Tatjana, Ajda Lenardič, Alenka Nemec Svete, and Simon Horvat. "Supplementation with >Your< Iron Syrup Corrects Iron Status in a Mouse Model of Diet-Induced Iron Deficiency." Biology 10, no. 5 (2021): 357. http://dx.doi.org/10.3390/biology10050357.

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The objective of this study was to compare the effects of >Your< Iron Syrup, a novel oral liquid iron-containing food supplement, with the commonly prescribed iron sulphate (Fe-sulphate) in a mouse model of diet-induced iron deficiency. Standard inbred BALB/cOlaHsd mice were fed low-iron diet for 11 weeks to induce significant decrease in blood haemoglobin and haematocrit and were then supplemented by gavage with either >Your< Iron Syrup or Fe-sulphate for two weeks. In >Your< Iron Syrup group, several markers of iron deficiency, such as serum iron concentration, transferrin

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Duparc, Thibaut, François Briand, Charlotte Trenteseaux, et al. "Liraglutide improves hepatic steatosis and metabolic dysfunctions in a 3-week dietary mouse model of nonalcoholic steatohepatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 317, no. 4 (2019): G508—G517. http://dx.doi.org/10.1152/ajpgi.00139.2019.

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Nonalcoholic steatohepatitis (NASH) is an emerging health problem worldwide. However, efficacious pharmacological treatment for NASH is lacking. A major issue for preclinical evaluation of potential therapeutics for NASH is the limited number of appropriate animal models, i.e., models that do not require long-term dietary intervention and adequately mimic disease progression in humans. The present study aimed to evaluate a 3-wk dietary mouse model of NASH and validate it by studying the effects of liraglutide, a compound in advanced clinical development for NASH. C57BL6/J mice were fed a diet

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Al-Shekaili, Hilal H., Terri L. Petkau, Izabella Pena, et al. "A novel mouse model for pyridoxine-dependent epilepsy due to antiquitin deficiency." Human Molecular Genetics 29, no. 19 (2020): 3266–84. http://dx.doi.org/10.1093/hmg/ddaa202.

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Abstract Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disease caused by mutations in the ALDH7A1 gene leading to blockade of the lysine catabolism pathway. PDE is characterized by recurrent seizures that are resistant to conventional anticonvulsant treatment but are well-controlled by pyridoxine (PN). Most PDE patients also suffer from neurodevelopmental deficits despite adequate seizure control with PN. To investigate potential pathophysiological mechanisms associated with ALDH7A1 deficiency, we generated a transgenic mouse strain with constitutive genetic ablation of Ald

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Manrique, Camila, Guido Lastra, Francisco I. Ramirez-Perez та ін. "Endothelial Estrogen Receptor-α Does Not Protect Against Vascular Stiffness Induced by Western Diet in Female Mice". Endocrinology 157, № 4 (2016): 1590–600. http://dx.doi.org/10.1210/en.2015-1681.

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Abstract Consumption of a diet high in fat and refined carbohydrates (Western diet [WD]) is associated with obesity and insulin resistance, both major risk factors for cardiovascular disease (CVD). In women, obesity and insulin resistance abrogate the protection against CVD likely afforded by estrogen signaling through estrogen receptor (ER)α. Indeed, WD in females results in increased vascular stiffness, which is independently associated with CVD. We tested the hypothesis that loss of ERα signaling in the endothelium exacerbates WD-induced vascular stiffening in female mice. We used a novel m

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Leishangthem, Geeta Devi, Ulaganathan Mabalirajan, Vijay Pal Singh, Anurag Agrawal, Balaram Ghosh, and Amit Kumar Dinda. "Ultrastructural Changes of Airway in Murine Models of Allergy and Diet-Induced Metabolic Syndrome." ISRN Allergy 2013 (September 10, 2013): 1–11. http://dx.doi.org/10.1155/2013/261297.

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Studying ultrastructural changes could reveal novel pathophysiology of obese-asthmatic condition as existing concepts in asthma pathogenesis are based on the histological changes of the diseased airway. While asthma is defined in functional terms, the potential of electron microscopy (EM) in providing cellular and subcellular detail is underutilized. With this view, we have performed transmission EM in the lungs from allergic mice that show key features of asthma and high-fat- or high-fructose-fed mice that mimicked metabolic syndrome to illustrate the ultrastructural changes. The primary focu

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Engstrom, Laura W., Loretta Bober, Shu-Cheng Chen, et al. "Kinetic Assessment and Therapeutic Modulation of Metabolic and Inflammatory Profiles in Mice on a High-Fat and Cholesterol Diet." PPAR Research 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/970164.

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The kinetics of metabolic and inflammatory parameters associated with obesity were evaluated in a murine diet-induced obesity (DIO) model using a diet high in fat and cholesterol. Cellular infiltration and mediator production were assessed and shown to be therapeutically modulated by the PPARgamma agonist rosiglitazone. C57BL/6 mice were maintained on a 45% fat/0.12% cholesterol (HF/CH) or Chow diet for 3, 6, 16, or 27 weeks. Flow cytometry was employed to monitor peripheral blood monocytes and adipose tissue macrophages (ATM). Gene expression and protein analysis methods were used to evaluate

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Nakanishi, Keisuke, Kosuke Kaji, Mitsuteru Kitade, et al. "Exogenous Administration of Low-Dose Lipopolysaccharide Potentiates Liver Fibrosis in a Choline-Deficient l-Amino-Acid-Defined Diet-Induced Murine Steatohepatitis Model." International Journal of Molecular Sciences 20, no. 11 (2019): 2724. http://dx.doi.org/10.3390/ijms20112724.

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Various rodent models have been proposed for basic research; however, the pathogenesis of human nonalcoholic steatohepatitis (NASH) is difficult to closely mimic. Lipopolysaccharide (LPS) has been reported to play a pivotal role in fibrosis development during NASH progression via activation of toll-like receptor 4 (TLR4) signaling. This study aimed to clarify the impact of low-dose LPS challenge on NASH pathological progression and to establish a novel murine NASH model. C57BL/6J mice were fed a choline-deficient l-amino-acid-defined (CDAA) diet to induce NASH, and low-dose LPS (0.5 mg/kg) was

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Ngai, Ying Fai, Whitney L. Quong, Melissa B. Glier, et al. "Ldlr−/− Mice Display Decreased Susceptibility to Western-Type Diet-Induced Obesity Due to Increased Thermogenesis." Endocrinology 151, no. 11 (2010): 5226–36. http://dx.doi.org/10.1210/en.2010-0496.

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The low-density lipoprotein receptor (Ldlr) is a key molecule involved with lipid clearance. The Ldlr−/− mouse has been used extensively as a model for studying atherosclerosis. This study sought to characterize the energy balance phenotype of Ldlr−/− mice with respect to weight gain, body composition, energy expenditure (EE), glucose homeostasis, and leptin sensitivity. Adult Ldlr−/− mice and Ldlr+/+ controls on a C57Bl/6J background were fed either a chow or a high-fat, high-sucrose Western-type diet (WTD) for eight wk. Physiological studies of food intake, EE, activity, insulin sensitivity,

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Shepard, Blythe D., Hermann Koepsell, and Jennifer L. Pluznick. "Renal olfactory receptor 1393 contributes to the progression of type 2 diabetes in a diet-induced obesity model." American Journal of Physiology-Renal Physiology 316, no. 2 (2019): F372—F381. http://dx.doi.org/10.1152/ajprenal.00069.2018.

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Olfactory receptors are G protein-coupled receptors that serve to detect odorants in the nose. Additionally, these receptors are expressed in other tissues, where they have functions outside the canonical smell response. Olfactory receptor 1393 (Olfr1393) was recently identified as a novel regulator of Na+-glucose cotransporter 1 (Sglt1) localization in the renal proximal tubule. Glucose reabsorption in the proximal tubule (via Sglt1 and Sglt2) has emerged as an important contributor to the development of diabetes. Inhibition of Sglt2 is accepted as a viable therapeutic treatment option for pa

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Sengupta, Monideepa, Suomia Abuirqeba, Amina Kameric, et al. "A two-hit model of alcoholic liver disease that exhibits rapid, severe fibrosis." PLOS ONE 16, no. 3 (2021): e0249316. http://dx.doi.org/10.1371/journal.pone.0249316.

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Alcoholic liver disease (ALD) is responsible for an average of 50.4% and 44.2%of liver disease deaths among males and females respectively. Driven by alcohol misuse, ALD is often reversible by cessation of consumption. However, abstinence programs can have limited success at curtailing abuse, and the loss of life. ALD, therefore, remains a significant clinical challenge. There is a need for effective treatments that prevent or reverse alcohol-induced liver damage to complement or supplant behavioral interventions. Metabolic syndrome, which is disproportionally prevalent in ALD patients, accele

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Martin, Keith R., Michael P. Jokinen, Hayden P. Honeycutt, et al. "Tumor Spectrum in the p53 Heterozygous Zeta Globin-Promoted Tg.AC (v-Ha-ras) Bitransgenic Mouse Model." Toxicologic Pathology 32, no. 4 (2004): 418–25. http://dx.doi.org/10.1080/01926230490462129.

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The use of a bitransgenic mouse model for cancer is an effective approach for studying the impact of specific carcinogens and the occurrence of tissue-specific lesions. We studied the novel p53 heterozygous zeta globin-promoted Tg.AC (v-Ha-ras) mouse model because these mice contain a carcinogen-inducible ras oncogene and one functional p53 tumor suppressor allele, both of which occur frequently in human cancers. Our aim was to characterize the short-term control and chemically induced tumor spectrum in this novel model. Mice were placed on basal semipurified diet containing 20% soy protein fo

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Zeng, Qianhui, Nannan Wang, Yaru Zhang, et al. "Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice." International Journal of Molecular Sciences 22, no. 10 (2021): 5390. http://dx.doi.org/10.3390/ijms22105390.

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Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp

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Zhuhua, Zhang, Wang Zhiquan, Yang Zhen, et al. "A novel mice model of metabolic syndrome: the high-fat-high-fructose diet-fed ICR mice." Experimental Animals 64, no. 4 (2015): 435–42. http://dx.doi.org/10.1538/expanim.14-0086.

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Trogen, Greta, Joshua Bacon, Ying Li, et al. "Transgenic overexpression of CTRP3 prevents alcohol-induced hepatic triglyceride accumulation." American Journal of Physiology-Endocrinology and Metabolism 315, no. 5 (2018): E949—E960. http://dx.doi.org/10.1152/ajpendo.00050.2018.

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This study tested the ability of a novel adipose tissue derived cytokine, C1q TNF-related protein-3 (CTRP3), to prevent alcohol-induced hepatic lipid accumulation, or alcoholic fatty liver disease (ALD). Previous work has demonstrated that CTRP3 is effective at preventing high-fat diet-induced fatty liver; however, the potential of CTRP3 to inhibit ALD has not been explored. To test the potential protective effects of CTRP3, transgenic mice overexpressing CTRP3 (Tg) or wild-type littermates (WT) were subjected to one of two different models of ALD. In the first model, known as the NIAAA model,

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Avalos, Bryant, Donovan A. Argueta, Pedro A. Perez, Mark Wiley, Courtney Wood, and Nicholas V. DiPatrizio. "Cannabinoid CB1 Receptors in the Intestinal Epithelium Are Required for Acute Western-Diet Preferences in Mice." Nutrients 12, no. 9 (2020): 2874. http://dx.doi.org/10.3390/nu12092874.

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The endocannabinoid system plays an important role in the intake of palatable food. For example, endocannabinoid signaling in the upper small-intestinal epithelium is increased (i) in rats after tasting dietary fats, which promotes intake of fats, and (ii) in a mouse model of diet-induced obesity, which promotes overeating via impaired nutrient-induced gut–brain satiation signaling. We now utilized a combination of genetic, pharmacological, and behavioral approaches to identify roles for cannabinoid CB1Rs in upper small-intestinal epithelium in preferences for a western-style diet (WD, high-fa

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Ravinet Trillou, Christine, Michèle Arnone, Claire Delgorge, et al. "Anti-obesity effect of SR141716, a CB1 receptor antagonist, in diet-induced obese mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (2003): R345—R353. http://dx.doi.org/10.1152/ajpregu.00545.2002.

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Because the CB1 receptor antagonist SR141716 was previously reported to modulate food intake in rodents, we studied its efficacy in reducing obesity in a diet-induced obesity (DIO) model widely used for research on the human obesity syndrome. During a 5-wk treatment, SR141716 (10 mg · kg−1 · day−1orally) induced a transient reduction of food intake (−48% on week 1) and a marked but sustained reduction of body weight (−20%) and adiposity (−50%) of DIO mice. Furthermore, SR141716 corrected the insulin resistance and lowered plasma leptin, insulin, and free fatty acid levels. Most of these effect

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Fung, C., A. Brown, J. Cox, C. Callaway, R. McKnight, and R. Lane. "Novel thromboxane A2 analog-induced IUGR mouse model." Journal of Developmental Origins of Health and Disease 2, no. 5 (2011): 291–301. http://dx.doi.org/10.1017/s2040174411000535.

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Rodents, particularly rats, are used in the majority of intrauterine growth restriction (IUGR) research. An important tool that is lacking in this field is the ability to impose IUGR on transgenic mice. We therefore developed a novel mouse model of chronic IUGR using U-46619, a thromboxane A2 (TXA2) analog, infusion. TXA2 overproduction is prevalent in human pregnancies complicated by cigarette smoking, diabetes mellitus and preeclampsia. In this model, U-46619 micro-osmotic pump infusion in the last week of C57BL/6J mouse gestation caused maternal hypertension. IUGR pups weighed 15% less, had

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Karasawa, Hiroshi, Seiko Nagata-Goto, Kiyosumi Takaishi, and Yoshihiro Kumagae. "A novel model of type 2 diabetes mellitus based on obesity induced by high-fat diet in BDF1 mice." Metabolism 58, no. 3 (2009): 296–303. http://dx.doi.org/10.1016/j.metabol.2008.09.028.

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Yu, Yinghua, Yizhen Wu, Alexander Szabo, et al. "Teasaponin Reduces Inflammation and Central Leptin Resistance in Diet-Induced Obese Male Mice." Endocrinology 154, no. 9 (2013): 3130–40. http://dx.doi.org/10.1210/en.2013-1218.

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Chronic inflammation is involved in the pathogenesis of obesity and type 2 diabetes. Recently teasaponin, an extract from tea, has been shown to have antiinflammatory effects. We examined the effect of teasaponin on obesity, inflammation, glucose metabolism, and central leptin sensitivity in obese mice fed a high-fat (HF) diet for 16 weeks. Intraperitoneal injections of teasaponin (10 mg/kg, daily) for 21 days significantly decreased the food intake and body weight of HF diet-induced obese mice. Teasaponin treatment also reduced the protein levels of proinflammatory cytokines (TNF-α, IL-6, and

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Sullivan, Timothy, Zhenhua Miao, Daniel J. Dairaghi, et al. "CCR2 antagonist CCX140-B provides renal and glycemic benefits in diabetic transgenic human CCR2 knockin mice." American Journal of Physiology-Renal Physiology 305, no. 9 (2013): F1288—F1297. http://dx.doi.org/10.1152/ajprenal.00316.2013.

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Chemokine (C-C motif) receptor 2 (CCR2) is central for the migration of monocytes into inflamed tissues. The novel CCR2 antagonist CCX140-B, which is currently in two separate phase 2 clinical trials in diabetic nephropathy, has recently been shown to reduce hemoglobin A1c and fasting blood glucose levels in type 2 diabetics. In this report, we describe the effects of this compound on glycemic and renal function parameters in diabetic mice. Since CCX140-B has a low affinity for mouse CCR2, transgenic human CCR2 knockin mice were generated and rendered diabetic with either a high-fat diet (diet

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Adam, Kieran, Alina Iuga, Anna S. Tocheva, and Adam Mor. "A novel mouse model for checkpoint inhibitor-induced adverse events." PLOS ONE 16, no. 2 (2021): e0246168. http://dx.doi.org/10.1371/journal.pone.0246168.

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Immune checkpoint inhibitors have demonstrated significant efficacy in the treatment of a variety of cancers, however their therapeutic potential is limited by abstruse immune related adverse events. Currently, no robust animal model exists of checkpoint inhibitor-induced adverse events. Establishing such a model will improve our mechanistic understanding of this process, which in turn will inform design of improved therapies. We developed a mouse model to determine inflammatory toxicities in response to dual checkpoint blockade in the presence of syngeneic tumors. Mice from susceptible geneti

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Park, Insun, Linda K. Johnson, Allaura Cox, et al. "Hypermethioninemia Leads to Fatal Bleeding and Increased Mortality in a Transgenic I278T Mouse Model of Homocystinuria." Biomedicines 8, no. 8 (2020): 244. http://dx.doi.org/10.3390/biomedicines8080244.

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Severely elevated plasma homocysteine and methionine lead to thromboembolic events and strokes in homocystinuric (HCU) patients. Mouse models of HCU failed to exhibit prothrombotic phenotype, presumably due to lack of hypermethioninemia. We evaluated the impact of hypermethioninemia together with hyperhomocysteinemia on murine HCU phenotype and compared the efficacy of the current and novel therapies for HCU. High methionine intake decreased survival of I278T mice, which died from intestinal bleeding with hepatic and pancreatic failure. I278T mice on normal or increased methionine intake devel

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Ma, Yong, Hongmei Jiang, Jun Fang, and Gang Liu. "IRW and IQW Reduce Colitis-Associated Cancer Risk by Alleviating DSS-Induced Colonic Inflammation." BioMed Research International 2019 (October 24, 2019): 1–9. http://dx.doi.org/10.1155/2019/6429845.

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Background and Objective. Bioactive peptides exert great influence in animals and human health by targeting gastrointestinal tracts. The colitis model of mice was induced by dextran sulfate sodium (DSS). Thirty-two 8-week-old mice weighing 23 g on average were randomly assigned to four groups of 8 each: mice fed basal diet (CON), mice fed basal diet with 5% DSS (DSS), mice fed 0.03% IRW with 5% DSS (IRW-DSS), and mice fed 0.03% IRW with 5% DSS (IQW-DSS). After an adaptation period of 3 days, on day 8, all mice were slaughtered. Serum samples were collected to determine the level of amino acids

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Cole, Banumathi K., Margaret A. Morris, Wojciech J. Grzesik, Kendall A. Leone, and Jerry L. Nadler. "Adipose Tissue-Specific Deletion of 12/15-Lipoxygenase Protects Mice from the Consequences of a High-Fat Diet." Mediators of Inflammation 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/851798.

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Type 2 diabetes is associated with obesity, insulin resistance, and inflammation in adipose tissue. 12/15-Lipoxygenase (12/15-LO) generates proinflammatory lipid mediators, which induce inflammation in adipose tissue. Therefore we investigated the role of 12/15-LO activity in mouse white adipose tissue in promoting obesity-induced local and systemic inflammatory consequences. We generated a mouse model for fat-specific deletion of 12/15-LO,aP2-Cre;12/15-LOloxP/loxP, which we call ad-12/15-LO mice, and placed wild-type controls and ad-12/15-LO mice on a high-fat diet for 16 weeks and examined o

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Kakehashi, Anna, Arpamas Chariyakornkul, Shugo Suzuki, et al. "Cache Domain Containing 1 Is a Novel Marker of Non-Alcoholic Steatohepatitis-Associated Hepatocarcinogenesis." Cancers 13, no. 6 (2021): 1216. http://dx.doi.org/10.3390/cancers13061216.

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In the present study, potential molecular biomarkers of NASH hepatocarcinogenesis were investigated using the STAM mice NASH model, characterized by impaired insulin secretion and development of insulin resistance. In this model, 2-days-old C57BL/6N mice were subjected to a single subcutaneous (s.c.) injection of 200 μg streptozotocin (STZ) to induce diabetes mellitus (DM). Four weeks later, mice were administered high-fat diet (HFD) HFD-60 for 14 weeks (STAM group), or fed control diet (STZ group). Eighteen-week-old mice were euthanized to allow macroscopic, microscopic, histopathological, im

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Hodgson, Kelly A., Brenda L. Govan, Anna K. Walduck, Natkunam Ketheesan, and Jodie L. Morris. "Impaired Early Cytokine Responses at the Site of Infection in a Murine Model of Type 2 Diabetes and Melioidosis Comorbidity." Infection and Immunity 81, no. 2 (2012): 470–77. http://dx.doi.org/10.1128/iai.00930-12.

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ABSTRACTBacterial infections are a common and serious complication of type 2 diabetes (T2D). The prevalence of melioidosis, an emerging tropical infection caused by the Gram-negative bacteriumBurkholderia pseudomallei, is increased in people with T2D. This is the first study to compare murine models of T2D and melioidosis. Susceptibility and disease progression following infection withB. pseudomalleiwere compared in our diet-induced polygenic mouse model and a leptin receptor-deficient monogenic model of T2D. The metabolic profile of mice with diet-induced diabetes, including body weight, bloo

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Liu, Yu, Fei Cheng, Yuxuan Luo та ін. "PEGylated Curcumin Derivative Attenuates Hepatic Steatosis via CREB/PPAR-γ/CD36 Pathway". BioMed Research International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/8234507.

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Curcumin has the potential to cure dyslipidemia and nonalcoholic fatty liver disease (NAFLD). However, its therapeutic effects are curbed by poor bioavailability. Our previous work has shown that modification of curcumin with polyethylene glycol (PEG) improves blood concentration and tissue distribution. This study sought to investigate the role of a novel PEGylated curcumin derivative (Curc-mPEG454) in regulating hepatic lipid metabolism and to elucidate the underlying molecular mechanism in a high-fat-diet- (HFD-) fed C57BL/6J mouse model. Mice were fed either a control chow diet (D12450B),

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Olivari, Violante, Maria Rosa Lidonnici, Mariateresa Pettinato, et al. "Targeting Transferrin Receptor 2: A Novel "Erythropoiesis-Stimulating Approach" in a Model of Anemia of Chronic Kidney Disease." Blood 134, Supplement_1 (2019): 956. http://dx.doi.org/10.1182/blood-2019-125783.

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Introduction Anemia is a common and invalidating complication of chronic kidney disease (CKD) mainly due to the impaired erythropoietin (EPO) production that parallels the progression of kidney failure. The current treatment, based on erythropoiesis-stimulating agents (ESA), is far from optimal, because of potential off-target side effects. The same holds true for HIF-stabilizers tested in phase 3 clinical trials. For this reason, the identification of agents that selectively boost erythropoiesis would be of great benefit. Transferrin Receptor 2 (TFR2) is a protein expressed in hepatocytes, wh

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Brown, Jacob D., Scott P. Naples, and Frank W. Booth. "Effects of voluntary running on oxygen consumption, RQ, and energy expenditure during primary prevention of diet-induced obesity in C57BL/6N mice." Journal of Applied Physiology 113, no. 3 (2012): 473–78. http://dx.doi.org/10.1152/japplphysiol.00668.2011.

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Diet-induced obesity (DIO) in C57BL/6 mice is the standard model for studying obesity in mice. The few reports of DIO utilizing voluntary running provide contradictory results with respect to prevention of obesity. However, total energy expenditures associated with voluntary running during DIO are unknown. We hypothesized that voluntary running would increase the amount of total energy expended during DIO. Female C57BL/6N mice were randomly assigned to one of three experimental groups [high-fat diet with voluntary running (HFRun); high-fat diet without running (HFSed); and low-fat diet without

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Xu, Dengqiu, Xiaofei Huang, Hozeifa M. Hassan, et al. "Hypoglycaemic effect of catalpol in a mouse model of high-fat diet-induced prediabetes." Applied Physiology, Nutrition, and Metabolism 45, no. 10 (2020): 1127–37. http://dx.doi.org/10.1139/apnm-2020-0075.

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Type 2 diabetes mellitus is a major health problem and a societal burden. Individuals with prediabetes are at increased risk of type 2 diabetes mellitus. Catalpol, an iridoid glycoside, has been reported to exert a hypoglycaemic effect in db/db mice, but its effect on the progression of prediabetes is unclear. In this study, we established a mouse model of prediabetes and examined the hypoglycaemic effect, and the mechanism of any such effect, of catalpol. Catalpol (200 mg/(kg·day)) had no effect on glucose tolerance or the serum lipid level in a mouse model of impaired glucose tolerance-stage

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Gibson, Breanne H., Matthew T. Duvernay, Stephen Gondek, and Jonathan G. Schoenecker. "132 A Novel Murine Model of Burn-Induced Platelet Dysfunction." Journal of Burn Care & Research 42, Supplement_1 (2021): S88—S89. http://dx.doi.org/10.1093/jbcr/irab032.136.

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Abstract Introduction Platelet dysfunction has been demonstrated as a part of burn induced coagulopathy (BIC), however, the etiology and clinical significance are unknown. Determining the etiology and clinical significance of BIC platelet dysfunction is difficult in humans due to heterogeneity of injuries and treatment. The goal of this study was to develop a murine model of BIC burn-induced platelet dysfunction to allow for high-throughput investigation of the mechanisms and the possible effects platelet dysfunction has on burn outcomes. Methods Using an established murine model of burn injur

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