Experimental Models of Alimentary Obesity in Rats

Байрашева, В. К.; Пчелин, И. Ю.; Егорова, А. Э.; Василькова, О. Н.; Корнюшин, О. В.

doi:10.32415/jscientia.2019.09-10.02

Juvenis scientia

2019

DOI: 10.32415/jscientia.2019.09-10.02

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Experimental Models of Alimentary Obesity in Rats

В. К. Байрашева

И. Ю. Пчелин

А. Э. Егорова

et al.

Abstract: Among existing genetic and non-genetic models of obesity, the most widely used are the models of diet-induced obesity in rodents due to their relatively easy reproducibility and similarities to human pathogenesis of obesity. Within this review, we provide the analysis of diet-induced obesity models in rats, highlight attractive strengths as well as disadvantages of high-fat diets, fat or sugar choice diets, “cafeteria diets”, and “western diet”. Potential obesogenic mechanisms of the discussed models are analy… Show more

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Cited by 4 publications

References 33 publications

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Endothelial dysfunction of the mesenteric arteries of rats in the early obesity induced by high-fat diet

Pan’kova

2022

Obes. metabol.

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Background: Disturbance of the morphological and functional properties of the vascular bed in obesity are a serious clinical problem. Basis to their development is endothelial dysfunction. The developed models of obesity in animals using various diets indicate a change in vascular reactivity, however, questions about the stage at which this occurs and what mechanisms are involved in this process remain open, while they are decisive for choosing the correct tactics for correcting dysfunctions.Aim: The aim of the present study is to determine the changes in acetylcholine (ACh)-induced vasodilation of isolated arteries from rats after six weeks of administration of a high-fat diet (HFD).Materials and methods: The experiments were performed on Sprague-Dawley males, which at the age of 8 weeks were divided into 2 experimental groups that were treated for the next 6 weeks in the following manner: 1 - control) with standard dry food; 2 - a group fed with a HFD, the total amount of fat in which was 50%. At finish of the diet, the degree of obesity, biochemical parameters in the blood, and blood pressure were measured. Intravital microscopy of the rat mesentery with video recording was used to study the reactivity of the vessels. The contractile and relaxant responses of the vessels were determined by changes in their diameter.Results: The rats after treatment with the HFD (n=15) had higher body weight and amount of visceral fat, significantly increased blood triglycerides, moderate increases in glucose level in blood and systolic pressure compared with the control (n=15). Relaxation responses of mesenteric arteries, having a diameter of 140 to 300 μm in PSS, were recorded after precontraction by phenylephrine. A decrease in ACh-induced vasorelaxation was obtained, which manifests itself before the development of significant changes in carbohydrate metabolism. Incubation of drugs with the inhibitor of endothelial NO synthase L-NAME led to a pronounced weakening of relaxation in animals on a standard diet, and had little effect on vasodilation in the arteries of rats with the HFD. Vasodilation induced by the administration of sodium nitroprusside (NO donor) did not differ significantly in control and experimental animals, which indicates that the sensitivity of vascular smooth muscle to NO remained practically unchanged. ACh-induced relaxation of arteries in dietary rats did not change when the cyclooxygenase pathway was blocked by diclofenac.Conclusion: Functional changes in the contractile activity of the mesenteric arteries, manifested in the form of a decrease in ACh-induced vasorelaxation, occur after treatment with the HFD when animals had an early stage of obesity development before the onset of pronounced disorders of carbohydrate metabolism. This decrease is mainly due to the disruption of the NO-dependent mechanism underlying ACh-induced relaxation in the norm.

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Endothelial dysfunction of the mesenteric arteries of rats in the early obesity induced by high-fat diet

Pan’kova

2022

Obes. metabol.

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High-fat, high-carbohydrate diet-induced experimental model of metabolic syndrome in rats

et al. 2021

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РЕЗЮМЕЦель. Разработать экспериментальную модель метаболического синдрома (МС) у крыс на основе высокожировой и высокоуглеводной диеты. Материалы и методы.Исследование выполнено на 20 самцах крыс линии Вистар, которые были распределены на контрольную и опытную группы. Крысы контрольной группы находились на стандартной диете. Крысы опытной группы в течение 12 нед получали высокожировую и высокоуглеводную диету, содержащую животный жир (17%), фруктозу (17%) и 20%-й раствор фруктозы вместо питьевой воды. В конце исследования у животных измеряли массу тела, артериальное давление (АД), проводили глюкозотолерантный (ГТТ) и инсулинотолерантный (ИТТ) тесты. В плазме крови определяли отдельные показатели липидного обмена, в печени -содержание триацилглицеролов (ТАГ) и холестерина (ХС).Результаты. Содержание животных на высокожировой и высокоуглеводной диете в течение 12 нед приводило к повышению АД, увеличению удельной массы висцеральной жировой ткани. Выполнение ГТТ и ИТТ позволило выявить у крыс с МС гипергликемию, нарушение толерантности к глюкозе и инсулинорезистентность. Было обнаружено увеличение концентрации ТАГ в плазме крови крыс опытной группы, при этом уровень общего ХС не отличался от контроля. У крыс с МС наблюдалось увеличение удельной массы печени, а также содержания в ней ТАГ и ХС.Заключение. Полученная экспериментальная модель диет-индуцированного метаболического синдрома воспроизводит большинство типичных признаков МС у человека и может быть полезна в изучении патофизиологических основ развития МС и методов его профилактики и лечения. Ключевые слова: метаболический синдром, высокожировая и высокоуглеводная диета, ожирение, дислипидемия, гипергликемия, инсулинорезистентность. Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов, связанных с публикацией настоящей статьи. Источник финансирования. Исследование выполнено при финансовой поддержке РФФИ и Томской области в рамках научного проекта № 19-415-703015 (№ 18-44-700009, 18-44703008) и Совета по грантам президента Российской Федерации (МК-143.2020.4). Соответствие принципам этики. Исследование выполнено с соблюдением принципов гуманности, изложенных в директивах Европейского сообщества (86/609/ЕЕС) и Хельсинкской декларации. Исследование одобрено локальным этическим комитетом СибГМУ (протокол № 7793 от 27.05.2019).

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Systemic inflammation markers of diet-induced metabolic syndrome in rat model

Birulina

Воронкова

Ivanov

et al. 2022

BRSMU

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Chronic systemic inflammation is essential in many chronic non-infectious diseases, including type 2 diabetes, obesity and metabolic syndrome (MS). This study aimed at characterization of systemic inflammatory reaction as a component of diet-induced MS in rat model. Thirty-three male Wistar rats were distributed into two groups designated 'control' (n = 15) and 'experimental (MS)' (n = 18). The groups were fed, respectively, regular and high-fat/high-carbohydrate diets for 12 weeks. The intensity of systemic inflammatory process against the background of metabolic impairments was assessed by total and differential counts of white blood cells and serum levels of total protein, C-reactive protein, cytokines (IL6, IL10 and TNFα), insulin and leptin. We also assessed the production of reactive oxygen species in adipose tissue samples. The experiment revealed signs of systemic inflammation in MS as compared to control, including reactive leukocytosis, hyperproteinemia and increased serum levels of C-reactive protein (2.6-fold; р = 0.001), IL10 (3.7-fold; р = 0.029) and TNFα (4.2-fold; р = 0.035). The observed changes were accompanied by elevated metabolic activity of visceral adipose tissue, indicated by hyperleptinemia and increased free radical oxidation intensity. Pairwise positive correlations of serum levels were revealed for leptin and insulin (r = 0.701; р = 0.001) and leptin and IL10 (r = 0.523; р = 0.012). Thus, high-fat/ high-carbohydrate diet promoted metabolic impairments concomitantly with early signs of systemic inflammation characteristic of MS and obesity.

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Experimental Models of Alimentary Obesity in Rats

Cited by 4 publications

References 33 publications

Endothelial dysfunction of the mesenteric arteries of rats in the early obesity induced by high-fat diet

Endothelial dysfunction of the mesenteric arteries of rats in the early obesity induced by high-fat diet

High-fat, high-carbohydrate diet-induced experimental model of metabolic syndrome in rats

Systemic inflammation markers of diet-induced metabolic syndrome in rat model

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