Oral ethinylestradiol–levonorgestrel therapy counteracts fructose-induced renal metabolic impairment in female rats

Kehinde Samuel Olaniyi , Isaiah Woru Sabinari , Lawrence Aderemi Olatunji
{"title":"Oral ethinylestradiol–levonorgestrel therapy counteracts fructose-induced renal metabolic impairment in female rats","authors":"Kehinde Samuel Olaniyi ,&nbsp;Isaiah Woru Sabinari ,&nbsp;Lawrence Aderemi Olatunji","doi":"10.1016/j.endmts.2021.100099","DOIUrl":null,"url":null,"abstract":"<div><p>Background: The excessive intake of fructose (FRD) induces insulin resistance (IR)-associated renal impairment. Similarly, the use of estrogen-progestin oral contraceptive therapy (EEL) has been associated with cardiometabolic syndrome, and its non-contraceptive benefits particularly in metabolic pathologies remain inconclusive. Therefore, the present study investigated the effects of EEL on renal metabolic function in rats exposed to FRD.</p><p>Methods: Female rats received vehicle (po), EEL (1.0 µg ethinylestradiol+5.0 µg levonorgestrel.), fructose (10%; w/v) and EEL+FRD respectively for 8 weeks. All data were expressed as means ± SEM and significance were accepted at <em>p</em>&lt;0.05.</p><p>Results: Data revealed that FRD/EEL caused IR with correspondent increased plasma/renal lipid, decreased glucose-6-dehydrogenase (G6PD), glutathione (GSH) and renal NO/adenosine. FRD but not EEL increased (<em>p</em>&lt;0.05) renal glycogen and decreased (<em>p</em>&lt;0.05) plasma NO/adenosine and pancreatic beta-cell function. These alterations were attenuated when EEL was administered with FRD.</p><p>Conclusion: The study demonstrates that FRD causes renal impairments accompanied by deficient NO/adenosine concentration and defective G6PD/GSH-dependent antioxidant defense. The findings also suggest that EEL blots the renal effects of FRD.</p></div>","PeriodicalId":34427,"journal":{"name":"Endocrine and Metabolic Science","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.endmts.2021.100099","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrine and Metabolic Science","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666396121000224","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

Background: The excessive intake of fructose (FRD) induces insulin resistance (IR)-associated renal impairment. Similarly, the use of estrogen-progestin oral contraceptive therapy (EEL) has been associated with cardiometabolic syndrome, and its non-contraceptive benefits particularly in metabolic pathologies remain inconclusive. Therefore, the present study investigated the effects of EEL on renal metabolic function in rats exposed to FRD.

Methods: Female rats received vehicle (po), EEL (1.0 µg ethinylestradiol+5.0 µg levonorgestrel.), fructose (10%; w/v) and EEL+FRD respectively for 8 weeks. All data were expressed as means ± SEM and significance were accepted at p<0.05.

Results: Data revealed that FRD/EEL caused IR with correspondent increased plasma/renal lipid, decreased glucose-6-dehydrogenase (G6PD), glutathione (GSH) and renal NO/adenosine. FRD but not EEL increased (p<0.05) renal glycogen and decreased (p<0.05) plasma NO/adenosine and pancreatic beta-cell function. These alterations were attenuated when EEL was administered with FRD.

Conclusion: The study demonstrates that FRD causes renal impairments accompanied by deficient NO/adenosine concentration and defective G6PD/GSH-dependent antioxidant defense. The findings also suggest that EEL blots the renal effects of FRD.

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
口服炔雌醇-左炔诺孕酮治疗可抵消果糖诱导的雌性大鼠肾脏代谢损伤
背景:过量摄入果糖(FRD)可诱导胰岛素抵抗(IR)相关的肾脏损害。同样,使用雌激素-黄体酮口服避孕药治疗(EEL)与心脏代谢综合征有关,其非避孕益处,特别是在代谢病理方面仍不确定。因此,本研究探讨了EEL对FRD暴露大鼠肾脏代谢功能的影响。方法:雌性大鼠给药(po)、EEL(1.0µg炔雌醇+5.0µg左炔诺孕酮)、果糖(10%;w/v)和EEL+FRD分别治疗8周。所有数据以均数±SEM表示,显著性以p<0.05接受。结果:数据显示,FRD/EEL引起IR,相应的血浆/肾脏脂质升高,葡萄糖-6-脱氢酶(G6PD)、谷胱甘肽(GSH)和肾脏NO/腺苷降低。FRD升高了肾糖原(p < 0.05),降低了血浆NO/腺苷和胰岛β细胞功能(p < 0.05)。当与FRD一起给药时,这些改变减弱。结论:研究表明,FRD引起肾损害,并伴有NO/腺苷浓度不足和G6PD/ gsh依赖性抗氧化防御缺陷。研究结果还表明,EEL可以抑制FRD对肾脏的影响。
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
Endocrine and Metabolic Science
Endocrine and Metabolic Science Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.80
自引率
0.00%
发文量
4
审稿时长
84 days
期刊最新文献
Long-term diabetic hyperglycaemia modifies social behaviour in rats Platelet activation and inflammation in transgender women using hormone therapy Prevalence of thyroid dysfunction among pregnant women in the horn of Africa: A systematic review and Meta-analysis Increase of serum vitamin D levels in the COVID-19 pandemic: Report of a Mexican reference clinical laboratory Hypoalbuminemia on admission in diabetic patients correlates with severity of illness in COVID-19: A retrospective clinical study and literature review
×
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