Characteristics of WBN/Kob diabetic fatty rats supplemented with a fructose-rich diet as a metabolic syndrome model: response to a GLP-1 receptor agonist

Namekawa, Junichi; Nemoto, Sayaka; Sunada, Gaku; Takanashi, Yuki; Fujio, Sakurako; Shirai, Mitsuyuki; Asai, Fumitoshi

doi:10.1292/jvms.18-0306

Cited by 3 publications

(3 citation statements)

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“…Similarly, in the present study, we found a significant reduction in plasma glucose levels and glucose tolerance aggravated by HFD supplementation in WBKDF rats. These anti‐hyperglycemic effects of liraglutide were probably due to its insulinotropic action …”

Section: Discussionsupporting

confidence: 92%

“…They received subcutaneous injections of either saline or liraglutide (Victoza; Novo Nordisk Pharma) at doses of 75 or 300 μg/kg body weight once daily for 4 weeks. The doses of liraglutide were determined according to results from previous studies . Blood samples were taken once weekly from the tail vein of nonfasting and conscious rats and plasma was used for glucose measurement.…”

Section: Methodsmentioning

confidence: 99%

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Effects of liraglutide on metabolic syndrome in WBN/Kob diabetic fatty rats supplemented with a high‐fat diet

Kaji

Takagi

Matsuda

et al. 2020

Anim Models and Exp Med

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Anim Models Exp Med. 2020;3:62-68. wileyonlinelibrary.com/journal/ame2 | INTRODUC TI ONMetabolic syndrome (MS) is an epidemic that represents a major health problem worldwide and is characterized by central obesity.The presence of abnormal metabolic parameters, such as central obesity, dyslipidemia, and hypertension, further increase the risk of cardiovascular death in MS. 1 The high prevalence of MS is probably due to the contemporary prevalence of obesity, unhealthy diet, and sedentary lifestyle. 2 Weight loss of 5%-10% has been shown to reduce complications related to obesity and improve the quality of life. 3 However, weight loss is difficult to maintain with lifestyle intervention alone. 4This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. AbstractBackground: Liraglutide, a GLP-1 receptor agonist, has recently been used to treat metabolic syndrome (MS) because of its anti-diabetic and anti-obesity effects. We have previously shown that Wistar Bonn Kobori diabetic and fatty (WBN/Kob-Lepr fa , WBKDF) rats fed a high-fat diet (HFD) developed MS including marked obesity, hyperglycemia, and dyslipidemia. To obtain further information on WBKDF-HFD rats as a severe MS model, we performed a pharmacological investigation into the anti-MS effects of liraglutide in this model. Methods:Seven-week-old male WBKDF-HFD rats were allocated to three groups (n = 8 in each group): a vehicle group, a low-dose liraglutide group, and a high-dose liraglutide group. They received subcutaneous injections of either saline or liraglutide at doses of 75 or 300 μg/kg body weight once daily for 4 weeks. Results:Results showed that liraglutide treatment reduced body weight gain and food intake in a dose-dependent manner. The marked hyperglycemia and the glucose tolerance were also significantly ameliorated in the liraglutide-treated groups. Moreover, liraglutide also reduced the plasma triglyceride concentration and liver fat accumulation. Conclusions:The present study demonstrated that liraglutide could significantly alleviate MS in WBKDF-HFD rats, and the reaction to liraglutide is similar to human patients with MS. WBKDF-HFD rats are therefore considered to be a useful model for research on severe human MS. K E Y W O R D Sdiabetes mellitus, liraglutide, metabolic syndrome, models, animal, obesity | 63 KAJI et Al.

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Effects of liraglutide on metabolic syndrome in WBN/Kob diabetic fatty rats supplemented with a high‐fat diet

Kaji

Takagi

Matsuda

et al. 2020

Anim Models and Exp Med

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“…WBN/Kob diabetic fatty rats represent a congenic strain carrying the fa allele of the leptin receptor gene (Lepr) that exhibits obesity, insulin resistance, and diabetes (62,63). WBN/Kob diabetic fatty rats fed a high-fructose diet for 4 weeks showed significant diffuse fatty degeneration (64). In addition, WBN/Kob diabetic fatty rats fed a high-fat diet for 4 weeks showed diffuse fatty changes with hepatocellular hypertrophy (65).…”

Section: Genetic Nafld/nash Rat Modelsmentioning

confidence: 99%

Pathophysiological Features of Rat Models of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

SAIGO,

UNO,

ISHIGURE

et al. 2024

In Vivo

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Nonalcoholic fatty liver disease (NAFLD)/ nonalcoholic steatohepatitis (NASH) is caused by various factors, including genetic and/or environmental factors, and has complicated pathophysiological features during the development of the disease. NAFLD/NASH is recognized as an unmet medical need, and NAFLD/NASH animal models are essential tools for developing new therapies, including potential drugs and biomarkers. In this review, we describe the pathological features of the NAFLD/NASH rat models, focusing on the histopathology of hepatic fibrosis. NAFLD/NASH rat models are divided into three categories: diet-induced, genetic, and combined models based on diet, chemicals, and genetics. Rat models of NASH with hepatic fibrosis are especially expected to contribute to the development of new therapies, such as drugs and biomarkers.The liver is the largest organ in the human body and performs various functions to maintain human health. Hepatic abnormalities in fatty liver disease include steatosis and steatosis-related liver damage. There are two types of fatty liver disease: alcoholic and nonalcoholic. Alcoholic fatty liver disease is caused by heavy alcohol consumption. However, the factors and mechanisms involved in the development of nonalcoholic fatty liver disease (NAFLD) are not fully understood. If not managed, both types of fatty liver disease progress to cirrhosis and liver cancer via hepatitis. NAFLD is a common liver disease worldwide with an alarmingly rapid prevalence (1-3). NAFLD is histopathologically classified as nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). NASH is a severe condition characterized by necroinflammation that progresses to cirrhosis and liver cancer. Animal models of NAFLD/NASH are pivotal in developing novel NAFLD/NASH therapies. The US Food and Drug Administration has provided guidance for the development of new drugs for the treatment of non-cirrhotic NASH with liver fibrosis, with no worsening of steatohepatitis and liver fibrosis as endpoints in clinical trials (https://www.fda.gov/media/119044/download). It is necessary to develop NAFLD/NASH models of hepatic inflammation/ fibrosis and to understand the pathophysiological features of these models. NAFLD/NASH models can be divided into three categories: genetic, dietary, and chemical. In this review, we focus on dietary and genetic rat models that exhibit hepatic pathological features. We also describe the pathological changes in the combined models based on genetics, diet, and chemicals. Diet-induced NAFLD/NASH Rat ModelsWestern diets and amino acid-modified diets are widely used to induce NAFLD/NASH-like lesions. Normal rats, such as Sprague-Dawley (SD) and Wistar rats, develop NAFLD/ NASH-like changes, including steatosis, inflammation, and fibrosis, chiefly caused by western-style diets. Fischer 344 (F344) rats also develop NASH-like lesions following a choline-deficient, methionine-lowered, L-amino acid-defined (CDAA) diet. Pathological characteristics of diet-induced NAFLD/NASH rat models are summariz...

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Diagnostic Criteria for Metabolic Syndrome in Diet-Induced Rodent Models: A Systematic Review

Virgen-Carrillo

Ríos

Torres

et al. 2021

CDR

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Background: Thousands of publications in recent years have addressed the induction of metabolic syndrome (MetS) in rodents, however, the criteria and the reference values for diagnosing this disease have not been defined. Objective: Our main objetive was to carry out a systematic review to gather evidence about the criteria for biochemical and anthropometric parameters in which scientific studies have relied to report that rats developed MetS from a previous dietary manipulation. Methods: We compiled characteristics and findings of diet induced MetS with high-fat, high-carbohydrate, high-fat/high-carbohydrates and cafeteria diet from PubMed and Science Direct databases published in the last 5 years. Results: The results on the principal determinants for the syndrome, published in the reviewed articles, were chosen to propose reference values in the rat models of food induction. Conclusion: The values obtained will serve as reference cut-of points in the development of the disease; in addition, the compilation of data will be useful in planning and executing research protocols in animal models.

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Characteristics of WBN/Kob diabetic fatty rats supplemented with a fructose-rich diet as a metabolic syndrome model: response to a GLP-1 receptor agonist

Cited by 3 publications

References 40 publications

Effects of liraglutide on metabolic syndrome in WBN/Kob diabetic fatty rats supplemented with a high‐fat diet

Effects of liraglutide on metabolic syndrome in WBN/Kob diabetic fatty rats supplemented with a high‐fat diet

Pathophysiological Features of Rat Models of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

Diagnostic Criteria for Metabolic Syndrome in Diet-Induced Rodent Models: A Systematic Review

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