Journal articles: 'Obesity – Animal models'

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Pomp, Daniel. "Animal models of obesity." Molecular Medicine Today 5, no. 10 (October 1999): 459–60. http://dx.doi.org/10.1016/s1357-4310(99)01580-4.

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Speakman, J., C. Hambly, S. Mitchell, and E. Król. "Animal models of obesity." Obesity Reviews 8, s1 (March 2007): 55–61. http://dx.doi.org/10.1111/j.1467-789x.2007.00319.x.

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Kasper, Christine E. "Animal Models of Exercise and Obesity." Annual Review of Nursing Research 31, no. 1 (October 2013): 1–17. http://dx.doi.org/10.1891/0739-6686.31.1.

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Animal models have been invaluable in the conduct of nursing research for the past 40 years. This review will focus on specific animal models that can be used in nursing research to study the physiologic phenomena of exercise and obesity when the use of human subjects is either scientifically premature or inappropriate because of the need for sampling tissue or the conduct of longitudinal studies of aging. There exists an extensive body of literature reporting the experimental use of various animal models, in both exercise science and the study of the mechanisms of obesity. Many of these studies are focused on the molecular and genetic mechanisms of organ system adaptation and plasticity in response to exercise, obesity, or both. However, this review will narrowly focus on the models useful to nursing research in the study of exercise in the clinical context of increasing performance and mobility, atrophy and bedrest, fatigue, and aging. Animal models of obesity focus on those that best approximate clinical pathology.

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Johnson, P. R., M. R. C. Greenwood, B. A. Horwitz, and J. S. Stern. "Animal Models of Obesity: Genetic Aspects." Annual Review of Nutrition 11, no. 1 (July 1991): 325–53. http://dx.doi.org/10.1146/annurev.nu.11.070191.001545.

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Joyner, Michael J. "Rethinking Animal Models and Human Obesity." Physiology 29, no. 6 (November 2014): 384–85. http://dx.doi.org/10.1152/physiol.00043.2014.

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York, David A. "LESSONS FROM ANIMAL MODELS OF OBESITY." Endocrinology and Metabolism Clinics of North America 25, no. 4 (December 1996): 781–800. http://dx.doi.org/10.1016/s0889-8529(05)70354-6.

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Segal-Lieberman, Gabriella, and Talma Rosenthal. "Animal Models in Obesity and Hypertension." Current Hypertension Reports 15, no. 3 (March 29, 2013): 190–95. http://dx.doi.org/10.1007/s11906-013-0338-3.

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Kanasaki, Keizo, and Daisuke Koya. "Biology of Obesity: Lessons from Animal Models of Obesity." Journal of Biomedicine and Biotechnology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/197636.

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Obesity is an epidemic problem in the world and is associated with several health problems, including diabetes, cardiovascular disease, respiratory failure, muscle weakness, and cancer. The precise molecular mechanisms by which obesity induces these health problems are not yet clear. To better understand the pathomechanisms of human disease, good animal models are essential. In this paper, we will analyze animal models of obesity and their use in the research of obesity-associated human health conditions and diseases such as diabetes, cancer, and obstructive sleep apnea syndrome.

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Ghanemi, Abdelaziz, Mayumi Yoshioka, and Jonny St-Amand. "Obese Animals as Models for Numerous Diseases: Advantages and Applications." Medicina 57, no. 5 (April 21, 2021): 399. http://dx.doi.org/10.3390/medicina57050399.

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With the advances in obesity research, a variety of animal models have been developed to investigate obesity pathogenesis, development, therapies and complications. Such obese animals would not only allow us to explore obesity but would also represent models to study diseases and conditions that develop with obesity or where obesity represents a risk factor. Indeed, obese subjects, as well as animal models of obesity, develop pathologies such as cardiovascular diseases, diabetes, inflammation and metabolic disorders. Therefore, obese animals would represent models for numerous diseases. Although those diseases can be induced in animals by chemicals or drugs without obesity development, having them developed as consequences of obesity has numerous advantages. These advantages include mimicking natural pathogenesis processes, using diversity in obesity models (diet, animal species) to study the related variabilities and exploring disease intensity and reversibility depending on obesity development and treatments. Importantly, therapeutic implications and pharmacological tests represent key advantages too. On the other hand, obesity prevalence is continuously increasing, and, therefore, the likelihood of having a patient suffering simultaneously from obesity and a particular disease is increasing. Thus, studying diverse diseases in obese animals (either induced naturally or developed) would allow researchers to build a library of data related to the patterns or specificities of obese patients within the context of pathologies. This may lead to a new branch of medicine specifically dedicated to the diseases and care of obese patients, similar to geriatric medicine, which focuses on the elderly population.

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Shore, Stephanie A. "Obesity and asthma: lessons from animal models." Journal of Applied Physiology 102, no. 2 (February 2007): 516–28. http://dx.doi.org/10.1152/japplphysiol.00847.2006.

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Epidemiological data indicate that obesity is a risk factor for asthma. These data are supported by observations in several murine models of obesity. Ob/ob, db/db, and Cpefatmice each exhibit innate airway hyperresponsiveness, a characteristic feature of asthma. These mice also respond more vigorously to common asthma triggers, including ozone. Here we discuss the implications of these data with respect to several mechanisms proposed to explain the relationship between obesity and asthma: 1) common etiologies; 2) comorbidities; 3) mechanical factors; and 4) adipokines. We focus on the role of adipokines, especially TNF-α, IL-6, leptin, and adiponectin. Understanding the mechanistic basis for the relationship between obesity and asthma may lead to novel therapeutic strategies for treatment of the obese asthmatic subject.

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Hariri, Niloofar, and Louise Thibault. "High-fat diet-induced obesity in animal models." Nutrition Research Reviews 23, no. 2 (October 27, 2010): 270–99. http://dx.doi.org/10.1017/s0954422410000168.

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Epidemiological studies have shown a positive relationship between dietary fat intake and obesity. Since rats and mice show a similar relationship, they are considered an appropriate model for studying dietary obesity. The present paper describes the history of using high-fat diets to induce obesity in animals, aims to clarify the consequences of changing the amount and type of dietary fats on weight gain, body composition and adipose tissue cellularity, and explores the contribution of genetics and sex, as well as the biochemical basis and the roles of hormones such as leptin, insulin and ghrelin in animal models of dietary obesity. The major factors that contribute to dietary obesity – hyperphagia, energy density and post-ingestive effects of the dietary fat – are discussed. Other factors that affect dietary obesity including feeding rhythmicity, social factors and stress are highlighted. Finally, we comment on the reversibility of high-fat diet-induced obesity.

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Kleinert, Maximilian, Christoffer Clemmensen, Susanna M. Hofmann, Mary C. Moore, Simone Renner, Stephen C. Woods, Peter Huypens, et al. "Animal models of obesity and diabetes mellitus." Nature Reviews Endocrinology 14, no. 3 (January 19, 2018): 140–62. http://dx.doi.org/10.1038/nrendo.2017.161.

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Trivedi, Premal S., and Lili A. Barouch. "Cardiomyocyte apoptosis in animal models of obesity." Current Hypertension Reports 10, no. 6 (November 23, 2008): 454–60. http://dx.doi.org/10.1007/s11906-008-0085-z.

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Xu, Wanying, Dominique Pepper, Junfeng Sun, Judith Welsh, Xizhong Cui, and Peter Q. Eichacker. "The Effects of Obesity on Outcome in Preclinical Animal Models of Infection and Sepsis: A Systematic Review and Meta-Analysis." Journal of Obesity 2020 (February 20, 2020): 1–13. http://dx.doi.org/10.1155/2020/1508764.

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Background. Clinical studies suggest obesity paradoxically increases survival during bacterial infection and sepsis but decreases it with influenza, but these studies are observational. By contrast, animal studies of obesity in infection can prospectively compare obese versus nonobese controls. We performed a systematic review and meta-analysis of animal investigations to further examine obesity’s survival effect in infection and sepsis. Methods. Databases were searched for studies comparing survival in obese versus nonobese animals following bacteria, lipopolysaccharide, or influenza virus challenges. Results. Twenty-one studies (761 obese and 603 control animals) met the inclusion criteria. Obesity reduced survival in 19 studies (11 significantly) and the odds ratio (95% CI) of survival (0.21(0.13, 0.35); I2 = 64%, p<0.01p < 0.01) but with high heterogeneity. Obesity reduced survival (1) consistently in both single-strain bacteria- and lipopolysaccharide-challenged studies (n = 6 studies, 0.21(0.13, 0.34); I2 = 31%, p=0.20 and n = 5, 0.22(0.13, 0.36); I2 = 0%, p=0.59, respectively), (2) not significantly with cecal ligation and puncture (n = 4, 0.72(0.08, 6.23); I2 = 75%, p<0.01), and (3) significantly with influenza but with high heterogeneity (n = 6, 0.12(0.04, 0.34); I2 = 73%, p<0.01). Obesity’s survival effects did not differ significantly comparing the four challenge types (p=0.49). Animal models did not include antimicrobials or glycemic control and study quality was low. Conclusions. Preclinical and clinical studies together emphasize the need for prospective studies in patients accurately assessing obesity’s impact on survival during severe infection.

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Thibault, Louise, Stephen C. Woods, and Margriet S. Westerterp-Plantenga. "The utility of animal models of human energy homeostasis." British Journal of Nutrition 92, S1 (August 2004): S41—S45. http://dx.doi.org/10.1079/bjn20041141.

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The prevalence of obesity among adults and children has increased steadily over the last few years worldwide, reaching epidemic proportions. Particularly alarming is the link between obesity and the development of chronic disorders such as heart disease, type 2 diabetes, hypertension and some cancers (Bjorntorp, 1997). Environmental causes of obesity are thought to include a sedentary lifestyle and an abundance of highly palatable energy-dense foods (Hill et al. 2003). Genetic factors also contribute to susceptibility to obesity, although the genetic basis of most human obesities is thought to be polygenic (Comuzzie & Allison, 1998; Barsh et al. 2000). The present paper considers some of the animal models used to infer aspects of human obesity, with an emphasis upon their usefulness.

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Seki, Yoshinori, Lyda Williams, Patricia M. Vuguin, and Maureen J. Charron. "Minireview: Epigenetic Programming of Diabetes and Obesity: Animal Models." Endocrinology 153, no. 3 (March 1, 2012): 1031–38. http://dx.doi.org/10.1210/en.2011-1805.

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A growing body of evidence suggests that the intrauterine (IU) environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life as put forth in the fetal origins of disease hypothesis. Metabolic diseases have been associated with alterations in the epigenome that occur without changes in the DNA sequence, such as cytosine methylation of DNA, histone posttranslational modifications, and micro-RNA. Animal models of epigenetic modifications secondary to an altered IU milieu are an invaluable tool to study the mechanisms that determine the development of metabolic diseases, such as diabetes and obesity. Rodent and nonlitter bearing animals are good models for the study of disease, because they have similar embryology, anatomy, and physiology to humans. Thus, it is feasible to monitor and modify the IU environment of animal models in order to gain insight into the molecular basis of human metabolic disease pathogenesis. In this review, the database of PubMed was searched for articles published between 1999 and 2011. Key words included epigenetic modifications, IU growth retardation, small for gestational age, animal models, metabolic disease, and obesity. The inclusion criteria used to select studies included animal models of epigenetic modifications during fetal and neonatal development associated with adult metabolic syndrome. Experimental manipulations included: changes in the nutritional status of the pregnant female (calorie-restricted, high-fat, or low-protein diets during pregnancy), as well as the father; interference with placenta function, or uterine blood flow, environmental toxin exposure during pregnancy, as well as dietary modifications during the neonatal (lactation) as well as pubertal period. This review article is focused solely on studies in animal models that demonstrate epigenetic changes that are correlated with manifestation of metabolic disease, including diabetes and/or obesity.

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West, David B. "GENETICS OF OBESITY IN HUMANS AND ANIMAL MODELS." Endocrinology and Metabolism Clinics of North America 25, no. 4 (December 1996): 801–13. http://dx.doi.org/10.1016/s0889-8529(05)70355-8.

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Mak, Robert H., Huey-Ju Kuo, and Wai W. Cheung. "Animal Models of Obesity-Associated Chronic Kidney Disease." Advances in Chronic Kidney Disease 13, no. 4 (October 2006): 374–85. http://dx.doi.org/10.1053/j.ackd.2006.07.003.

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Mavanji, Vijayakumar, Charles J. Billington, Catherine M. Kotz, and Jennifer A. Teske. "Sleep and obesity: A focus on animal models." Neuroscience & Biobehavioral Reviews 36, no. 3 (March 2012): 1015–29. http://dx.doi.org/10.1016/j.neubiorev.2012.01.001.

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Proietto, Joseph, and Anne W. Thorburn. "2 Animal models of obesity—theories of aetiology." Baillière's Clinical Endocrinology and Metabolism 8, no. 3 (July 1994): 509–25. http://dx.doi.org/10.1016/s0950-351x(05)80284-8.

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Lyons, M. J., K. Nagashima, and J. B. Zabriskie. "Animal models of postinfectious obesity: Hypothesis and review." Journal of Neurovirology 8, no. 1 (January 2002): 1–5. http://dx.doi.org/10.1080/135502802317247758.

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Haque, Md Rafiul, and Monika Dhaka. "A brief study of mechanism, animal models, and management for obesity." Current Research Journal of Pharmaceutical and Allied Sciences 4, no. 2 (September 30, 2021): 11–27. http://dx.doi.org/10.54059/2021.4(2)crjpas_192.

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Obesity appears as fat accumulation in adipose tissue from high energy intake and insufficient energy consumption. It is accompanied by several factors such as genetics, environmental, fetal nutrition, energy intake and expenditure, and culture. These factors stimulate several other mechanisms that contribute to obesity and obesity-related disorders such as hypertension, diabetes, arthritis, hyperlipidemia, coronary heart disease, etc. In the present article, we have examined the main factors, symptoms, and special problems associated with obesity, mechanisms of obesity, and the relation of important parameters with obesity. We have also depicted the various animal models for obesity research. Lastly, we have described the management of obesity.

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Martins, Tânia, Catarina Castro-Ribeiro, Sílvia Lemos, Tiago Ferreira, Elisabete Nascimento-Gonçalves, Eduardo Rosa, Paula Alexandra Oliveira, and Luís Miguel Antunes. "Murine Models of Obesity." Obesities 2, no. 2 (March 31, 2022): 127–47. http://dx.doi.org/10.3390/obesities2020012.

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Obesity, classified as an epidemic by the WHO, is a disease that continues to grow worldwide. Obesity results from abnormal or excessive accumulation of fat and usually leads to the development of other associated diseases, such as type 2 diabetes, hypertension, cancer, cardiovascular diseases, among others. In vitro and in vivo models have been crucial for studying the underlying mechanisms of obesity, discovering new therapeutic targets, and developing and validating new pharmacological therapies against obesity. Preclinical animal models of obesity comprise a variety of species: invertebrates, fishes, and mammals. However, small rodents are the most widely used due to their cost-effectiveness, physiology, and easy genetic manipulation. The induction of obesity in rats or mice can be achieved by the occurrence of spontaneous single-gene mutations or polygenic mutations, by genetic modifications, by surgical or chemical induction, and by ingestion of hypercaloric diets. In this review, we describe some of the most commonly used murine models in obesity research.

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Zhang, Xuwen, and David Val-Laillet. "Obesity Animal Models for Acupuncture and Related Therapy Research Studies." Evidence-Based Complementary and Alternative Medicine 2021 (September 30, 2021): 1–29. http://dx.doi.org/10.1155/2021/6663397.

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Obesity and related diseases are considered as pandemic representing a worldwide threat for health. Animal models are critical to validate the effects and understand the mechanisms related to classical or innovative preventive and therapeutic strategies. It is, therefore, important to identify the best animal models for translational research, using different evaluation criteria such as the face, construct, and predictive validity. Because the pharmacological treatments and surgical interventions currently used for treating obesity often present many undesirable side effects, relatively high relapse probabilities, acupuncture, electroacupuncture (EA), and related therapies have gained more popularity and attention. Many kinds of experimental animal models have been used for obesity research studies, but in the context of acupuncture, most of the studies were performed in rodent obesity models. Though, are these obesity rodent models really the best for acupuncture or related therapies research studies? In this study, we review different obesity animal models that have been used over the past 10 years for acupuncture and EA research studies. We present their respective advantages, disadvantages, and specific constraints. With the development of research on acupuncture and EA and the increasing interest regarding these approaches, proper animal models are critical for preclinical studies aiming at developing future clinical trials in the human. The aim of the present study is to provide researchers with information and guidance related to the preclinical models that are currently available to investigate the outcomes of acupuncture and related therapies.

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Fernandes, Melina Ribeiro, Nayara Vieira de Lima, Karoline Silva Rezende, Isabela Caroline Marques Santos, Iandara Schettert Silva, and Rita de Cássia Avellaneda Guimarães. "Animal models of obesity in rodents. An integrative review." Acta Cirurgica Brasileira 31, no. 12 (December 2016): 840–44. http://dx.doi.org/10.1590/s0102-865020160120000010.

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Schalling, M., J. Johansen, L. Nordfors, and F. Lönnqvist. "Genes involved in animal models of obesity and anorexia." Journal of Internal Medicine 245, no. 6 (June 1999): 613–19. http://dx.doi.org/10.1046/j.1365-2796.1999.00489.x.

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Speakman, John, Catherine Hambly, Sharon Mitchell, and Elżbieta Król. "The contribution of animal models to the study of obesity." Laboratory Animals 42, no. 4 (October 2008): 413–32. http://dx.doi.org/10.1258/la.2007.006067.

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Summary Obesity results from prolonged imbalance of energy intake and energy expenditure. Animal models have provided a fundamental contribution to the historical development of understanding the basic parameters that regulate the components of our energy balance. Five different types of animal model have been employed in the study of the physiological and genetic basis of obesity. The first models reflect single gene mutations that have arisen spontaneously in rodent colonies and have subsequently been characterized. The second approach is to speed up the random mutation rate artificially by treating rodents with mutagens or exposing them to radiation. The third type of models are mice and rats where a specific gene has been disrupted or overexpressed as a deliberate act. Such genetically-engineered disruptions may be generated through the entire body for the entire life (global transgenic manipulations) or restricted in both time and to certain tissue or cell types. In all these genetically-engineered scenarios, there are two types of situation that lead to insights: where a specific gene hypothesized to play a role in the regulation of energy balance is targeted, and where a gene is disrupted for a different purpose, but the consequence is an unexpected obese or lean phenotype. A fourth group of animal models concern experiments where selective breeding has been utilized to derive strains of rodents that differ in their degree of fatness. Finally, studies have been made of other species including non-human primates and dogs. In addition to studies of the physiological and genetic basis of obesity, studies of animal models have also informed us about the environmental aspects of the condition. Studies in this context include exploring the responses of animals to high fat or high fat/high sugar (Cafeteria) diets, investigations of the effects of dietary restriction on body mass and fat loss, and studies of the impact of candidate pharmaceuticals on components of energy balance. Despite all this work, there are many gaps in our understanding of how body composition and energy storage are regulated, and a continuing need for the development of pharmaceuticals to treat obesity. Accordingly, reductions in the use of animal models, while ethically desirable, will not be feasible in the short to medium term, and indeed an expansion in activity using animal models is anticipated as the epidemic continues and spreads geographically.

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Cowen, Neil, and Anish Bhatnagar. "The Potential Role of Activating the ATP-Sensitive Potassium Channel in the Treatment of Hyperphagic Obesity." Genes 11, no. 4 (April 21, 2020): 450. http://dx.doi.org/10.3390/genes11040450.

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To evaluate the potential role of ATP-sensitive potassium (KATP) channel activation in the treatment of hyperphagic obesity, a PubMed search was conducted focused on the expression of genes encoding the KATP channel, the response to activating the KATP channel in tissues regulating appetite and the establishment and maintenance of obesity, the evaluation of KATP activators in obese hyperphagic animal models, and clinical studies on syndromic obesity. KATP channel activation is mechanistically involved in the regulation of appetite in the arcuate nucleus; the regulation of hyperinsulinemia, glycemic control, appetite and satiety in the dorsal motor nucleus of vagus; insulin secretion by β-cells; and the synthesis and β-oxidation of fatty acids in adipocytes. KATP channel activators have been evaluated in hyperphagic obese animal models and were shown to reduce hyperphagia, induce fat loss and weight loss in older animals, reduce the accumulation of excess body fat in growing animals, reduce circulating and hepatic lipids, and improve glycemic control. Recent experience with a KATP channel activator in Prader–Willi syndrome is consistent with the therapeutic responses observed in animal models. KATP channel activation, given the breadth of impact and animal model and clinical results, is a viable target in hyperphagic obesity.

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Madhusudhan, Thati, and Wolfram Ruf. "Coagulation Signalling and Metabolic Disorders: Lessons Learned from Animal Models." Hämostaseologie 39, no. 02 (May 27, 2019): 164–72. http://dx.doi.org/10.1055/s-0039-1688800.

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AbstractNutrient excess in obesity drives metabolic reprogramming in multiple tissues involving extensive interorgan and intercellular crosstalk. Experimental and clinical studies show that prolonged nutrient excess often compromises metabolic adaptation propagating proobesogenic and proinflammatory responses. Chronic inflammation further promotes insulin resistance and associated comorbidities. Obesity and type 2 diabetes are characterized by a hypercoagulable state and clinical studies show a strong correlation of markers of coagulation activation in metabolic disorders. Coagulation protease-dependent signalling via protease-activated receptors is intimately associated with inflammation. The experimental evidence supports roles of tissue factor and G protein coupled protease-activated receptor-2 signalling in the regulation of insulin resistance and metabolic inflammation in diet-induced obesity. Likewise, increases in plasminogen activator inhibitor-1 levels and fibrin-driven inflammation promote insulin resistance in obesity. Additionally, impaired thrombomodulin-dependent protein C activation is mechanistically linked to diabetic kidney disease. Given the increased usage of direct oral anticoagulants, understanding the role of specific coagulation proteases in regulation of metabolic inflammation is highly relevant and might provide insights into the design of novel treatment regimens for patients suffering from thromboinflammatory and cardiometabolic disorders.

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Olsen, Magnus K., Helene Johannessen, Reshma Ramracheya, Chun-Mei Zhao, and Duan Chen. "New Approaches for Weight Loss: Experiments Using Animal Models." Current Pharmaceutical Design 24, no. 18 (September 12, 2018): 1926–35. http://dx.doi.org/10.2174/1381612824666180614075412.

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The number of people who are overweight and obese are continuously increasing both in the adult and adolescent populations. Coinciding with this is the increased prevalence of health problems such as type 2 diabetes (T2D). Bariatric surgery is the only proven long-term treatment of obesity and may induce remission of T2D, although the underlying mechanisms are unknown. The translational studies presented here might provide insight on the mechanism of steady-state energy balance of the obese phenotype using a special time-restricted feeding regimen for weight loss during the steady-state energy balance; mechanism by vagal blocking therapy (vBLoc® therapy) as a new treatment for obesity; and possible mechanism behind the remission of T2D following gastric bypass surgery.

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Li, M., D. M. Sloboda, and M. H. Vickers. "Maternal Obesity and Developmental Programming of Metabolic Disorders in Offspring: Evidence from Animal Models." Experimental Diabetes Research 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/592408.

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The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. Although an obesogenic nutritional environment and increasingly sedentary lifestyle contribute to our risk of developing obesity, a growing body of evidence links early life nutritional adversity to the development of long-term metabolic disorders. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring.

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Fricker, Lloyd D. "Neuropeptidomics to Study Peptide Processing in Animal Models of Obesity." Endocrinology 148, no. 9 (September 1, 2007): 4185–90. http://dx.doi.org/10.1210/en.2007-0123.

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Neuropeptidomics is the analysis of the neuropeptides present in a tissue extract. Most neuropeptidomic studies use mass spectrometry to detect and identify the peptides, which provides information on the precise posttranslationally modified form of each peptide. Quantitative peptidomics uses isotopic labels to compare the levels of peptides in extracts from two different samples. This technique is ideal for examining neuropeptide levels in a variety of systems and is especially suited for studies of mice lacking peptide-processing enzymes. This review is focused on the neuropeptidomics technique and its application to the analysis of mice with a mutation that inactivates carboxypeptidase E, a critical enzyme in the biosynthesis of many neuroendocrine peptides. Mice without carboxypeptidase E activity are overweight, and a key question is the identification of the peptide or peptides responsible. The quantitative peptidomics approach has provided some insights toward the answer to this question.

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West, D. B., and B. York. "Dietary fat, genetic predisposition, and obesity: lessons from animal models." American Journal of Clinical Nutrition 67, no. 3 (March 1, 1998): 505S—512S. http://dx.doi.org/10.1093/ajcn/67.3.505s.

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Picklo, Matthew J., and Eric Uthus. "Methionine Sulfoxide Disposition is Altered in Animal Models of Obesity." Free Radical Biology and Medicine 49 (January 2010): S40. http://dx.doi.org/10.1016/j.freeradbiomed.2010.10.082.

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Casper, Regina C., Elinor L. Sullivan, and Laurence Tecott. "Relevance of animal models to human eating disorders and obesity." Psychopharmacology 199, no. 3 (March 4, 2008): 313–29. http://dx.doi.org/10.1007/s00213-008-1102-2.

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Park, Hye-Sung, Jae-Heung Cho, Koh-Woon Kim, Won-Seok Chung, and Mi-Yeon Song. "Effects of Panax ginseng on Obesity in Animal Models: A Systematic Review and Meta-Analysis." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–16. http://dx.doi.org/10.1155/2018/2719794.

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Objective. To determine the antiobesity effects of Panax ginseng in animals. Methods. We conducted a systematic search for all controlled trials (up to March 2017) that assessed the antiobesity effects of P. ginseng in animal obesity models in the PubMed, EMBASE, Cochrane library, Web of Science, and Scopus databases. The primary outcome was final body weight measured at the longest follow-up time after administration of the intervention. The secondary outcome was the lipid profile. We assessed methodological quality using the SYRCLE risk of bias tool, and RevMan 5.3 was used to perform a meta-analysis. Finally, a subgroup analysis of parameters including intervention duration, animal models, and type of ginseng was performed. Result. We identified 16 studies that met the inclusion criteria. Data from the meta-analysis indicated that the intervention group had a significantly lower body weight than the control group (SMD: −1.50, 95% CI: −1.90 to −1.11, χ2: 78.14, P<0.0001, I2 = 58%). Final body weight was lower in an animal obesity model induced by high-fat diet than in genetic models. Also the intervention group had a significantly higher serum HDL level and lower serum LDL, TG, and TC level than the control group. Conclusion. Our meta-analysis indicated that oral administration of P. ginseng significantly inhibits weight gain and improves serum lipid profiles in animal obesity models. However, causes of obesity and type of ginseng may affect treatment effects.

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Reid, D. T., and B. Eksteen. "Murine models provide insight to the development of non-alcoholic fatty liver disease." Nutrition Research Reviews 28, no. 2 (October 23, 2015): 133–42. http://dx.doi.org/10.1017/s0954422415000128.

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AbstractAssociated with the obesity epidemic, non-alcoholic fatty liver disease (NAFLD) has become the leading liver disease in North America. Approximately 30 % of patients with NAFLD may develop non-alcoholic steatohepatitis (NASH) that can lead to cirrhosis and hepatocellular carcinoma (HCC). Frequently animal models are used to help identify underlying factors contributing to NAFLD including insulin resistance, dysregulated lipid metabolism and mitochondrial stress. However, studying the inflammatory, progressive nature of NASH in the context of obesity has proven to be a challenge in mice. Although the development of effective treatment strategies for NAFLD and NASH is gaining momentum, the field is hindered by a lack of a concise animal model that reflects the development of liver disease during obesity and the metabolic syndrome. Therefore, selecting an animal model to study NAFLD or NASH must be done carefully to ensure the optimal application. The most widely used animal models have been reviewed highlighting their advantages and disadvantages to studying NAFLD and NASH specifically in the context of obesity.

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Shabbir, Faizania, M. Mazhar Hussain, and Tausif Ahmed Rajput. "OBESITY." Professional Medical Journal 22, no. 06 (June 10, 2015): 683–389. http://dx.doi.org/10.29309/tpmj/2015.22.06.1231.

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Objective: To study the effects of atorvastatin administration on serum IL-6,WBC and platelet count in obese male and female animal models. Study Design: Randomizedcontrol trial (RCT). Place and duration of study: The study was conducted at Department ofPhysiology, Army Medical College, Rawalpindi in collaboration with National Institute of Health(NIH), Islamabad and Centre for Research in Experimental and Applied Medicine (CREAM),Army Medical College, Rawalpindi for funding, blood sampling and biochemical assaysrespectively. Material and Methods: Ninety healthy male and female Sprague Dawley ratswere selected and randomly divided into three equal groups. Group I rats were fed normal dietfor a period of three weeks. Group II rats were fed high fat diet for a period of three weeks toinduce obesity. Group III rats were administered atorvastatin 10 mg/kg/day orally by gavagemethod for three weeks after obesity induction. Terminal sampling by intra-cardiac puncturewas done at the end of study. Whole blood was used to perform blood complete picture by KX21 Sysmex Hematology Analyzer which includes platelet count and WBC count and serum wasused to measure IL-6 levels by Enzyme Linked Immunosorbant Assay (ELISA). Results: Therewas a significant decrease (p<0.05) in serum IL-6 levels and WBC count, whereas platelet countwas not significantly (p>0.05) affected by atorvastatin administration. Conclusions: Althoughatorvastatin reduces obesity related inflammation by decreasing serum IL-6 levels and WBCcount, it has no effect on platelet count in male and female obese animal models.

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Von Diemen, Vinicius, Eduardo Neubarth Trindade, and Manoel Roberto Maciel Trindade. "Experimental model to induce obesity in rats." Acta Cirurgica Brasileira 21, no. 6 (December 2006): 425–29. http://dx.doi.org/10.1590/s0102-86502006000600013.

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The etiology of obesity is multifactorial and is becoming a problem of public health, due to its increased prevalence and the consequent repercussion of its comorbidities on the health of the population. The great similarity and homology between the genomes of rodents and humans make these animal models a major tool to study conditions affecting humans, which can be simulated in rats. Obesity can be induced in animals by neuroendocrine, dietary or genetic changes. The most widely used models to induce obesity in rats are a lesion of the ventromedial hypothalamic nucleus (VMH) by administering monosodium glutamate or a direct electrical lesion, ovariectomy, feeding on hypercaloric diets and genetic manipulation for obesity.

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Tomankova, Veronika, Pavel Anzenbacher, and Eva Anzenbacherova. "Effects of obesity on liver cytochromes P450 in various animal models." Biomedical Papers 161, no. 2 (June 14, 2017): 144–51. http://dx.doi.org/10.5507/bp.2017.026.

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Crandall, David L., and Peter Cervoni. "Assessment of Animal Models for Investigating the Cardiovascular Adaptations to Obesity." Pathology and Immunopathology Research 6, no. 4 (1987): 284–300. http://dx.doi.org/10.1159/000157059.

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Thorner, Michael O. "Growth hormone insensitivity and obesity: Insights from human and animal models." Obesity Research & Clinical Practice 3, no. 1 (March 2009): 1–2. http://dx.doi.org/10.1016/j.orcp.2009.01.002.

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Fernández-Quintela, Alfredo, Christian Carpéné, Maialen Fernández, Leixuri Aguirre, Iñaki Milton-Laskibar, José Contreras, and Maria P. Portillo. "Anti-obesity effects of resveratrol: comparison between animal models and humans." Journal of Physiology and Biochemistry 73, no. 3 (August 2016): 417–29. http://dx.doi.org/10.1007/s13105-016-0544-y.

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Hayden, Melvin R., and James R. Sowers. "Childhood-Adolescent Obesity in the Cardiorenal Syndrome: Lessons from Animal Models." Cardiorenal Medicine 1, no. 2 (2011): 75–86. http://dx.doi.org/10.1159/000327022.

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Vickers, Steven P., Helen C. Jackson, and Sharon C. Cheetham. "The utility of animal models to evaluate novel anti-obesity agents." British Journal of Pharmacology 164, no. 4 (October 2011): 1248–62. http://dx.doi.org/10.1111/j.1476-5381.2011.01245.x.

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Vatashchuk, Myroslava V., Maria M. Bayliak, Viktoria V. Hurza, Kenneth B. Storey, and Volodymyr I. Lushchak. "Metabolic Syndrome: Lessons from Rodent and Drosophila Models." BioMed Research International 2022 (June 22, 2022): 1–13. http://dx.doi.org/10.1155/2022/5850507.

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Overweight and obesity are health conditions tightly related to a number of metabolic complications collectively called “metabolic syndrome” (MetS). Clinical diagnosis of MetS includes the presence of the increased waist circumference or so-called abdominal obesity, reduced high density lipoprotein level, elevated blood pressure, and increased blood glucose and triacylglyceride levels. Different approaches, including diet-induced and genetically induced animal models, have been developed to study MetS pathogenesis and underlying mechanisms. Studies of metabolic disturbances in the fruit fly Drosophila and mammalian models along with humans have demonstrated that fruit flies and small mammalian models like rats and mice have many similarities with humans in basic metabolic functions and share many molecular mechanisms which regulate these metabolic processes. In this paper, we describe diet-induced, chemically and genetically induced animal models of the MetS. The advantages and limitations of rodent and Drosophila models of MetS and obesity are also analyzed.

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Martins, Tânia, Tiago Ferreira, Elisabete Nascimento-Gonçalves, Catarina Castro-Ribeiro, Sílvia Lemos, Eduardo Rosa, Luís Miguel Antunes, and Paula Alexandra Oliveira. "Obesity Rodent Models Applied to Research with Food Products and Natural Compounds." Obesities 2, no. 2 (April 6, 2022): 171–204. http://dx.doi.org/10.3390/obesities2020015.

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Obesity is a disease whose incidence has increased over the last few decades. Despite being a multifactorial disease, obesity results essentially from excessive intake of high-calorie foods associated with low physical activity. The demand for a pharmacological therapy using natural compounds as an alternative to synthetic drugs has increased. Natural compounds may have few adverse effects and high economic impact, as most of them can be extracted from underexploited plant species and food by-products. To test the potential anti-obesogenic effects of new natural substances, the use of preclinical animal models of obesity has been an important tool, among which rat and mouse models are the most used. Some animal models are monogenic, such as the db/db mice, ob/ob mice, Zucker fatty rat and Otsuka Long-Evans Tokushima fatty rat. There are also available chemical models using the neurotoxin monosodium glutamate that induces lesions in the ventromedial hypothalamus nucleus, resulting in the development of obesity. However, the most widely used are the obesity models induced by high-fat diets. The aim of this review was to compile detail studies on the anti-obesity effects of natural compounds or their derivatives on rodent models of obesity as well as a critical analysis of the data.

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Berger, Claudia, and Nora Klöting. "Leptin Receptor Compound Heterozygosity in Humans and Animal Models." International Journal of Molecular Sciences 22, no. 9 (April 25, 2021): 4475. http://dx.doi.org/10.3390/ijms22094475.

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Leptin and its receptor are essential for regulating food intake, energy expenditure, glucose homeostasis and fertility. Mutations within leptin or the leptin receptor cause early-onset obesity and hyperphagia, as described in human and animal models. The effect of both heterozygous and homozygous variants is much more investigated than compound heterozygous ones. Recently, we discovered a spontaneous compound heterozygous mutation within the leptin receptor, resulting in a considerably more obese phenotype than described for the homozygous leptin receptor deficient mice. Accordingly, we focus on compound heterozygous mutations of the leptin receptor and their effects on health, as well as possible therapy options in human and animal models in this review.

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Olsen, Magnus Kringstad, Helene Johannessen, Nikki Cassie, Perry Barrett, Koji Takeuchi, Bård Kulseng, Duan Chen, and Chun-Mei Zhao. "Steady-state energy balance in animal models of obesity and weight loss." Scandinavian Journal of Gastroenterology 52, no. 4 (December 20, 2016): 442–49. http://dx.doi.org/10.1080/00365521.2016.1267791.

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COLLIER, GREG, KEN WALDER, ANDREA SILVA, JANETTE TENNE-BROWN, ANDREW SANIGORSKI, DAVID SEGAL, LAKSHMI KANTHAM, and GUY AUGERT. "New Approaches to Gene Discovery with Animal Models of Obesity and Diabetes." Annals of the New York Academy of Sciences 967, no. 1 (January 24, 2006): 403–13. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04296.x.

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Journal articles on the topic 'Obesity – Animal models'

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