Effects of Aging on Secreted Adipocytokines in Visceral Fat of Female C3H/HeJ Mice Consuming a Long-Term High-Fat Diet

Dietetics Pub Date : 2024-06-13 DOI:10.3390/dietetics3020016
Noshin Mubtasim, Benjamin Barr, Caleb Boren, Lauren Gollahon
{"title":"Effects of Aging on Secreted Adipocytokines in Visceral Fat of Female C3H/HeJ Mice Consuming a Long-Term High-Fat Diet","authors":"Noshin Mubtasim, Benjamin Barr, Caleb Boren, Lauren Gollahon","doi":"10.3390/dietetics3020016","DOIUrl":null,"url":null,"abstract":"The excess consumption of a high-fat diet has been identified as one of the factors contributing to obesity. Women are at higher risk of adult obesity than men, predisposing them to a different set of detrimental disease conditions. Furthermore, aging studies show that physiological decline also has a serious impact on changes in the endocrine properties of white adipose tissue. However, there is still relatively little known about the factors associated with obesity and aging and their compounding impacts on women’s health. To investigate changes in adipocytokine secretion profiles, obesity was induced in female C3H/HeJ mice through the long-term consumption of a high-fat diet. Weight gain measurements and the Echo MRI analysis of fat composition showed that increases were due solely to the high fat content in the diet. Adipocytokine secretions were analyzed in media conditioned from harvested visceral fat tissue that was organ-cultured ex vivo. Adipocytokine analysis performed across diets and ages showed that there were significant increases in Adiponectin and Leptin secretion in high-fat diets, accelerating increases in Resistin secretion in high-fat diets. Aging induced the increased secretion of Lipcalin-2, Pentraxin-3, Serpin E1, MCP-1, and ICAM-1, regardless of diet. Furthermore, the comparisons of organoid-cultured protein secretions and flash-frozen tissue samples differed greatly, suggesting the WAT organoid cultures may yield information that is more reflective of in situ conditions. Taken together, our results show that high-fat diets and aging in C3H/HeJ female mice significantly impact secretions from adipose tissue, which may contribute to women’s health issues.","PeriodicalId":503963,"journal":{"name":"Dietetics","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Dietetics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/dietetics3020016","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The excess consumption of a high-fat diet has been identified as one of the factors contributing to obesity. Women are at higher risk of adult obesity than men, predisposing them to a different set of detrimental disease conditions. Furthermore, aging studies show that physiological decline also has a serious impact on changes in the endocrine properties of white adipose tissue. However, there is still relatively little known about the factors associated with obesity and aging and their compounding impacts on women’s health. To investigate changes in adipocytokine secretion profiles, obesity was induced in female C3H/HeJ mice through the long-term consumption of a high-fat diet. Weight gain measurements and the Echo MRI analysis of fat composition showed that increases were due solely to the high fat content in the diet. Adipocytokine secretions were analyzed in media conditioned from harvested visceral fat tissue that was organ-cultured ex vivo. Adipocytokine analysis performed across diets and ages showed that there were significant increases in Adiponectin and Leptin secretion in high-fat diets, accelerating increases in Resistin secretion in high-fat diets. Aging induced the increased secretion of Lipcalin-2, Pentraxin-3, Serpin E1, MCP-1, and ICAM-1, regardless of diet. Furthermore, the comparisons of organoid-cultured protein secretions and flash-frozen tissue samples differed greatly, suggesting the WAT organoid cultures may yield information that is more reflective of in situ conditions. Taken together, our results show that high-fat diets and aging in C3H/HeJ female mice significantly impact secretions from adipose tissue, which may contribute to women’s health issues.
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
衰老对长期高脂饮食雌性 C3H/HeJ 小鼠内脏脂肪中分泌的脂肪细胞因子的影响
过量摄入高脂肪饮食已被确认为导致肥胖的因素之一。与男性相比,女性成年后患肥胖症的风险更高,容易引发一系列不同的有害疾病。此外,衰老研究表明,生理机能的衰退也会严重影响白色脂肪组织内分泌特性的变化。然而,人们对肥胖和衰老的相关因素及其对女性健康的复合影响仍然知之甚少。为了研究脂肪细胞因子分泌曲线的变化,研究人员通过长期食用高脂肪饮食诱导雌性 C3H/HeJ 小鼠肥胖。体重增加的测量结果和对脂肪成分的回声核磁共振成像分析表明,体重增加完全是由于饮食中脂肪含量过高所致。脂肪细胞因子分泌物是在从体内器官培养的内脏脂肪组织中获取的培养基中进行分析的。对不同饮食和年龄段的脂肪细胞因子进行的分析表明,高脂肪饮食中的脂肪连素和瘦素分泌显著增加,高脂肪饮食中的抗脂素分泌加速增加。无论饮食如何,衰老都会诱导脂联素-2、五肽-3、血清素 E1、MCP-1 和 ICAM-1 的分泌增加。此外,类器官培养的蛋白质分泌物与急冻组织样本的比较结果差别很大,这表明WAT类器官培养物可能会产生更能反映原位条件的信息。总之,我们的研究结果表明,C3H/HeJ雌性小鼠的高脂饮食和衰老会显著影响脂肪组织的分泌,这可能会导致女性的健康问题。
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
自引率
0.00%
发文量
0
期刊最新文献
Biomarkers for Assessing Diet-Related Neurocognitive Deficits in Children—A Systematic Review Dietary Habits and Caries Prevalence in Older Adults: A Scoping Review Monitoring the Mineral Content of Plant Foods in Food Composition Databases Effect of a Two-Week Diet without Meat and Poultry on Serum Coenzyme Q10 Levels Effects of Aging on Secreted Adipocytokines in Visceral Fat of Female C3H/HeJ Mice Consuming a Long-Term High-Fat Diet
×
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