High fat intake aggravates hyperlipidemia and suppresses fatty liver symptoms induced by a high-sucrose diet in rats.

IF 5.1 1区 农林科学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Food & Function Pub Date : 2024-10-04 DOI:10.1039/d4fo00863d
Qi Song, Akari Kikumoto, Shumin Sun, Satoshi Mochizuki, Hiroaki Oda
{"title":"High fat intake aggravates hyperlipidemia and suppresses fatty liver symptoms induced by a high-sucrose diet in rats.","authors":"Qi Song, Akari Kikumoto, Shumin Sun, Satoshi Mochizuki, Hiroaki Oda","doi":"10.1039/d4fo00863d","DOIUrl":null,"url":null,"abstract":"<p><p>Overconsumption of sucrose or fat is widely acknowledged as a prominent feature of unhealthy dietary patterns. Both factors commonly co-occur and are recognized as hallmarks of the Western diet, which is an important contributor to non-communicative diseases. In this study, we investigated the hazards of high sucrose or fat intake, either alone or in combination. Wistar rats were divided into four groups and fed a control starch diet, high-sucrose diet, high-fat diet, or high-sucrose/fat diet for 30 days. High fat intake increased body weight and visceral and subcutaneous adipose tissue weights. Both high-sucrose and -fat diets were associated with increased plasma triglyceride and glucose levels, and high sucrose also elevated plasma cholesterol levels. The combination of high sucrose and fat synergistically elevated plasma triglyceride levels. The high-sucrose diet increased liver weight and hepatic total lipid and triglyceride levels, whereas this increase was suppressed by the high-fat diet. The high sucrose increased the mRNA levels of hepatic genes involved in fatty acid synthesis and transport (ACLY, ACACA, FAS, ELOVL6, SCD1, SREBP1, and CD36), whereas the high fat suppressed the high sucrose-induced expression of these genes. We observed that high sucrose and fat contents differently exerted their effects on hyperlipidemia and fatty liver. Furthermore, high fat aggravated hyperlipidemia and suppressed fatty liver induced by high sucrose.</p>","PeriodicalId":77,"journal":{"name":"Food & Function","volume":null,"pages":null},"PeriodicalIF":5.1000,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food & Function","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1039/d4fo00863d","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Overconsumption of sucrose or fat is widely acknowledged as a prominent feature of unhealthy dietary patterns. Both factors commonly co-occur and are recognized as hallmarks of the Western diet, which is an important contributor to non-communicative diseases. In this study, we investigated the hazards of high sucrose or fat intake, either alone or in combination. Wistar rats were divided into four groups and fed a control starch diet, high-sucrose diet, high-fat diet, or high-sucrose/fat diet for 30 days. High fat intake increased body weight and visceral and subcutaneous adipose tissue weights. Both high-sucrose and -fat diets were associated with increased plasma triglyceride and glucose levels, and high sucrose also elevated plasma cholesterol levels. The combination of high sucrose and fat synergistically elevated plasma triglyceride levels. The high-sucrose diet increased liver weight and hepatic total lipid and triglyceride levels, whereas this increase was suppressed by the high-fat diet. The high sucrose increased the mRNA levels of hepatic genes involved in fatty acid synthesis and transport (ACLY, ACACA, FAS, ELOVL6, SCD1, SREBP1, and CD36), whereas the high fat suppressed the high sucrose-induced expression of these genes. We observed that high sucrose and fat contents differently exerted their effects on hyperlipidemia and fatty liver. Furthermore, high fat aggravated hyperlipidemia and suppressed fatty liver induced by high sucrose.

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
高脂肪摄入会加重高脂血症,并抑制高蔗糖饮食诱发的大鼠脂肪肝症状。
过度摄入蔗糖或脂肪被公认为是不健康饮食模式的一个显著特征。这两种因素通常同时存在,被认为是西方饮食的标志,而西方饮食是导致非传染性疾病的重要因素。在这项研究中,我们调查了单独或同时摄入大量蔗糖或脂肪的危害。我们将 Wistar 大鼠分为四组,分别喂食对照淀粉饮食、高蔗糖饮食、高脂肪饮食或高蔗糖/脂肪饮食 30 天。高脂肪摄入会增加体重以及内脏和皮下脂肪组织的重量。高蔗糖和高脂饮食都会导致血浆甘油三酯和葡萄糖水平升高,高蔗糖还会使血浆胆固醇水平升高。高蔗糖和脂肪的组合协同提高了血浆甘油三酯水平。高蔗糖饮食增加了肝脏重量和肝脏总脂质及甘油三酯水平,而高脂肪饮食抑制了这种增加。高蔗糖增加了参与脂肪酸合成和转运的肝脏基因(ACLY、ACACA、FAS、ELOVL6、SCD1、SREBP1 和 CD36)的 mRNA 水平,而高脂肪抑制了高蔗糖诱导的这些基因的表达。我们观察到,高蔗糖和高脂肪对高脂血症和脂肪肝的影响是不同的。此外,高脂肪会加重高脂血症,抑制高蔗糖诱导的脂肪肝。
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
Food & Function
Food & Function BIOCHEMISTRY & MOLECULAR BIOLOGY-FOOD SCIENCE & TECHNOLOGY
CiteScore
10.10
自引率
6.60%
发文量
957
审稿时长
1.8 months
期刊介绍: Food & Function provides a unique venue for physicists, chemists, biochemists, nutritionists and other food scientists to publish work at the interface of the chemistry, physics and biology of food. The journal focuses on food and the functions of food in relation to health.
期刊最新文献
High fat intake aggravates hyperlipidemia and suppresses fatty liver symptoms induced by a high-sucrose diet in rats. Impact of complementary feeding on infant gut microbiome, metabolites and early development. The association between the amount and timing of coffee consumption with chronic kidney disease in diabetic patients. Correction: Gut-derived wild blueberry phenolic acid metabolites modulate extrinsic cutaneous damage. Nisin A elevates adenosine to achieve anti-inflammatory activity.
×
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