Interleukin-6-deficient mice are more susceptible to steatosis but resistant to inflammation and tumorigenesis in mice with long-term high-fat feeding
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- 英文论文题名：Interleukin-6-deficient mice are more susceptible to steatosis but resistant to inflammation and tumorigenesis in mice with long-term high-fat feeding
- 论文作者：Yin Shi ; Bertola Adeline ; Gual Philippe ; Gao Bin ; Wang Hua
- 英文论文作者：Yin Shi ; Bertola Adeline ; Gual Philippe ; Gao Bin ; Wang Hua ; Department of Geriatrics ; Affiliated Provincial Hospital of Anhui Medical University ; Laboratory of Liver Diseases ; National Institute on Alcohol Abuse and Alcoholism ; National Institutes of Health ; INSERM U895 ; C3M ; Batiment Universitaire ARCHIMED ; Department of Oncology ; The First Affiliated Hospital of Anhui Medical University
- 年：2016
- 作者机构：Department of Geriatrics,Affiliated Provincial Hospital of Anhui Medical University;Laboratory of Liver Diseases,National Institute on Alcohol Abuse and Alcoholism,National Institutes of Health;INSERM U895,C3M,Batiment Universitaire ARCHIMED;Department of Oncology,The First Affiliated Hospital of Anhui Medical University;
- 英文论文关键词：Interleukin-6 ; liver steatosis ; liver inflammation ; liver cancer
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R589.2;R735.7
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1301k
- 原文格式：D
- 会议级别：全国
摘要
Obesity is associated with an increased risk of hepatocellular carcinoma(HCC) development and associated with elevation of serum and hepatic interleukin-6(IL-6). Elevation of hepatic IL-6 levels correlates with the disease severity in patients with nonalcoholic fatty liver disease. Previous studies show that IL-6 promotes liver tumorigenesis induced by hepatic procarcinogene diethylnitrosamine plus high-fat diet feeding in mice. To specifically define the role of IL-6 in obesity-associated liver cancer, IL-6 knockout(IL-6KO) and wild-type C57BL/6 mice were fed either control chow or a high-fat diet for 1 year to induce obesity and HCC. Hepatic steatosis, injury, inflammation, fibrosis and cancer were evaluated. Long-term high-fat diet feeding resulted in severe obesity, nonalcoholic steatohepatitis, and increased expression of hepatic IL-6 mRNA and its downstream STAT3 activation in wild-type C57BL/6 mice. Interestingly, around 60%(11/18) of these obese mice showed macroscopic tumor lesions, indicating that high-fat diet alone can initiate and promote HCC development. Compared with wild-type mice, IL-6KO mice had more severe liver injury, fibrosis and steatosis, but less inflammation and tumorigenesis after being fed a high-fat diet for one year. In conclusion, IL-6-deficent mice have more steatosis but less liver inflammation and tumorigenesis in the murine model of long-term high-fat diet feeding.
Obesity is associated with an increased risk of hepatocellular carcinoma(HCC) development and associated with elevation of serum and hepatic interleukin-6(IL-6). Elevation of hepatic IL-6 levels correlates with the disease severity in patients with nonalcoholic fatty liver disease. Previous studies show that IL-6 promotes liver tumorigenesis induced by hepatic procarcinogene diethylnitrosamine plus high-fat diet feeding in mice. To specifically define the role of IL-6 in obesity-associated liver cancer, IL-6 knockout(IL-6KO) and wild-type C57BL/6 mice were fed either control chow or a high-fat diet for 1 year to induce obesity and HCC. Hepatic steatosis, injury, inflammation, fibrosis and cancer were evaluated. Long-term high-fat diet feeding resulted in severe obesity, nonalcoholic steatohepatitis, and increased expression of hepatic IL-6 mRNA and its downstream STAT3 activation in wild-type C57BL/6 mice. Interestingly, around 60%(11/18) of these obese mice showed macroscopic tumor lesions, indicating that high-fat diet alone can initiate and promote HCC development. Compared with wild-type mice, IL-6KO mice had more severe liver injury, fibrosis and steatosis, but less inflammation and tumorigenesis after being fed a high-fat diet for one year. In conclusion, IL-6-deficent mice have more steatosis but less liver inflammation and tumorigenesis in the murine model of long-term high-fat diet feeding.
Obesity is associated with an increased risk of hepatocellular carcinoma(HCC) development and associated with elevation of serum and hepatic interleukin-6(IL-6). Elevation of hepatic IL-6 levels correlates with the disease severity in patients with nonalcoholic fatty liver disease. Previous studies show that IL-6 promotes liver tumorigenesis induced by hepatic procarcinogene diethylnitrosamine plus high-fat diet feeding in mice. To specifically define the role of IL-6 in obesity-associated liver cancer, IL-6 knockout(IL-6KO) and wild-type C57BL/6 mice were fed either control chow or a high-fat diet for 1 year to induce obesity and HCC. Hepatic steatosis, injury, inflammation, fibrosis and cancer were evaluated. Long-term high-fat diet feeding resulted in severe obesity, nonalcoholic steatohepatitis, and increased expression of hepatic IL-6 mRNA and its downstream STAT3 activation in wild-type C57BL/6 mice. Interestingly, around 60%(11/18) of these obese mice showed macroscopic tumor lesions, indicating that high-fat diet alone can initiate and promote HCC development. Compared with wild-type mice, IL-6KO mice had more severe liver injury, fibrosis and steatosis, but less inflammation and tumorigenesis after being fed a high-fat diet for one year. In conclusion, IL-6-deficent mice have more steatosis but less liver inflammation and tumorigenesis in the murine model of long-term high-fat diet feeding.
引文