A diet high in glucose and deficient in dietary fibre causes fat accumulation in the liver without weight gain

IF 2.3 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Biochemistry and Biophysics Reports Pub Date : 2024-10-19 DOI:10.1016/j.bbrep.2024.101848
Sonoko Karino , Haruki Usuda , Shoma Kanda , Takayuki Okamoto , Tomomi Niibayashi , Takahisa Yano , Kohji Naora , Koichiro Wada
{"title":"A diet high in glucose and deficient in dietary fibre causes fat accumulation in the liver without weight gain","authors":"Sonoko Karino ,&nbsp;Haruki Usuda ,&nbsp;Shoma Kanda ,&nbsp;Takayuki Okamoto ,&nbsp;Tomomi Niibayashi ,&nbsp;Takahisa Yano ,&nbsp;Kohji Naora ,&nbsp;Koichiro Wada","doi":"10.1016/j.bbrep.2024.101848","DOIUrl":null,"url":null,"abstract":"<div><div>This study investigated whether a standard calorie diet that is high in glucose and deficient in dietary fibre (described as HGD [high glucose diet]) induces hepatic fat accumulation in mice. We evaluated hepatic steatosis at 7 days and 14 days after the commencement of the HGD. Hepatic triglycerides and areas of oil droplets increased in the HGD group both at day 7 and day 14, whereas weight gain, weight of epididymal fat, and plasma levels of triglycerides were unaffected by HGD consumption. A microarray analysis of the livers revealed that the expression of lipogenesis-related genes was the most affected by HGD consumption. Furthermore, HGD consumption induced the expression of hepatic proteins of fatty acid synthetase, acetyl-CoA carboxylase alpha, and stearoyl-CoA desaturase 1, which are known to be involved in the synthesis of triglyceride. These results indicate that HGD consumption causes fat accumulation in the liver, with an increase in enzymes that are involved in de novo lipogenesis without an accompanying weight or obesity phenotype. Our new findings suggest that HGD consumption could serve as a breeding ground for liver steatosis.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101848"},"PeriodicalIF":2.3000,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry and Biophysics Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2405580824002127","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

This study investigated whether a standard calorie diet that is high in glucose and deficient in dietary fibre (described as HGD [high glucose diet]) induces hepatic fat accumulation in mice. We evaluated hepatic steatosis at 7 days and 14 days after the commencement of the HGD. Hepatic triglycerides and areas of oil droplets increased in the HGD group both at day 7 and day 14, whereas weight gain, weight of epididymal fat, and plasma levels of triglycerides were unaffected by HGD consumption. A microarray analysis of the livers revealed that the expression of lipogenesis-related genes was the most affected by HGD consumption. Furthermore, HGD consumption induced the expression of hepatic proteins of fatty acid synthetase, acetyl-CoA carboxylase alpha, and stearoyl-CoA desaturase 1, which are known to be involved in the synthesis of triglyceride. These results indicate that HGD consumption causes fat accumulation in the liver, with an increase in enzymes that are involved in de novo lipogenesis without an accompanying weight or obesity phenotype. Our new findings suggest that HGD consumption could serve as a breeding ground for liver steatosis.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
高葡萄糖和缺乏膳食纤维的饮食会导致脂肪在肝脏堆积,但体重不会增加
本研究调查了高葡萄糖和缺乏膳食纤维的标准热量饮食(称为 HGD [高葡萄糖饮食])是否会诱发小鼠肝脏脂肪堆积。我们在 HGD 开始后的 7 天和 14 天对肝脏脂肪变性进行了评估。HGD组小鼠肝脏甘油三酯和油滴面积在第7天和第14天均有所增加,而体重增加、附睾脂肪重量和血浆甘油三酯水平则不受HGD影响。对肝脏进行的芯片分析表明,摄入 HGD 对脂肪生成相关基因的表达影响最大。此外,摄入 HGD 会诱导肝脏中脂肪酸合成酶、乙酰-CoA 羧化酶 alpha 和硬脂酰-CoA 去饱和酶 1 蛋白的表达,而已知这些蛋白参与了甘油三酯的合成。这些结果表明,摄入 HGD 会导致脂肪在肝脏中蓄积,参与新脂肪生成的酶会增加,但不会伴随体重或肥胖表型。我们的新发现表明,摄入 HGD 可能成为肝脏脂肪变性的温床。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Biochemistry and Biophysics Reports
Biochemistry and Biophysics Reports Biochemistry, Genetics and Molecular Biology-Biophysics
CiteScore
4.60
自引率
0.00%
发文量
191
审稿时长
59 days
期刊介绍: Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.
期刊最新文献
Application of liposomal nanoparticles of berberine in photodynamic therapy of A549 lung cancer spheroids NOS3 regulates angiogenic potential of human induced pluripotent stem cell-derived endothelial cells StarD5 modulates B cell cholesterol synthesis and IgG1 plasma cell differentiation Molecular dynamics studies reveal the structural impacts of LRRK2 R1441C and LRRK2 D1994A mutations in Parkinson's disease An immortalized adipose-derived stem cells line from the PIK3CA-related overgrowth spectrum: Unveiling novel therapeutic targets
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1