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肥胖诱导癌症的小鼠模型。

Murine Model of Obesity-Induced Cancer.

作者信息

Badi Niharika, Cruz-Monserrate Zobeida

机构信息

Department of Internal Medicine, Division of Gastroenterology, Hepatology, and Nutrition, and Arthur G. James Comprehensive Cancer Center, The Ohio State University Wexner Medical Center, Columbus, OH, USA.

出版信息

Methods Mol Biol. 2022;2435:195-201. doi: 10.1007/978-1-0716-2014-4_14.

DOI:10.1007/978-1-0716-2014-4_14
PMID:34993948
Abstract

Obesity is a major risk factor for the development of multiple cancers. In efforts to develop models that will assist the scientific community in studying the mechanisms of this risk, a diet-induced obesity model of obesity is often utilized. Here we describe the use of diet-induced obesity (DIO) diets to study the effects of high-fat diet weight gain in the context of cancer mouse models.

摘要

肥胖是多种癌症发生的主要风险因素。为了开发有助于科学界研究这种风险机制的模型,人们经常使用饮食诱导肥胖模型。在此,我们描述了在癌症小鼠模型背景下,使用饮食诱导肥胖(DIO)饮食来研究高脂饮食体重增加的影响。

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Murine Model of Obesity-Induced Cancer.肥胖诱导癌症的小鼠模型。
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2
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本文引用的文献

1
Vital Signs: Trends in Incidence of Cancers Associated with Overweight and Obesity - United States, 2005-2014.生命体征:2005 - 2014年美国超重和肥胖相关癌症发病率趋势
MMWR Morb Mortal Wkly Rep. 2017 Oct 3;66(39):1052-1058. doi: 10.15585/mmwr.mm6639e1.
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Incidence of pancreatic cancer is dramatically increased by a high fat, high calorie diet in KrasG12D mice.在携带KrasG12D突变的小鼠中,高脂肪、高热量饮食会显著增加胰腺癌的发病率。
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Lipocalin-2 Promotes Pancreatic Ductal Adenocarcinoma by Regulating Inflammation in the Tumor Microenvironment.
脂质运载蛋白-2通过调节肿瘤微环境中的炎症促进胰腺导管腺癌。
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A high-fat diet activates oncogenic Kras and COX2 to induce development of pancreatic ductal adenocarcinoma in mice.高脂肪饮食激活致癌性 Kras 和 COX2,诱导小鼠胰腺导管腺癌的发生。
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High-fat diet-induced obesity in animal models.高脂肪饮食诱导的动物模型肥胖。
Nutr Res Rev. 2010 Dec;23(2):270-99. doi: 10.1017/S0954422410000168. Epub 2010 Oct 27.
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Rodent obesity models: an overview.啮齿动物肥胖模型:概述
Exp Clin Endocrinol Diabetes. 2001;109(6):307-19. doi: 10.1055/s-2001-17297.
10
Animal models of obesity: genetic aspects.肥胖的动物模型:遗传因素
Annu Rev Nutr. 1991;11:325-53. doi: 10.1146/annurev.nu.11.070191.001545.