The Impact of SGLT1 Inhibition on Frailty and Sarcopenia: A Mediation Mendelian Randomization Study

医学 孟德尔随机化 肌萎缩 握力 内科学 老年学 生理学 遗传学 基因 生物 基因型 遗传变异
作者
Byron Huang,Yujie Zhang,Guangfeng Ruan,Xing Yu,Qin Liu,M Zhang,YU Ming-zhong,Ai Chen,Y Z Liang,Liangdi Xie,Li Luo
出处
期刊:Journal of Cachexia, Sarcopenia and Muscle [Springer Science+Business Media]
标识
DOI:10.1002/jcsm.13614
摘要

ABSTRACT Background Although pharmacological effects of SGLT2 inhibitors on the development of frailty and sarcopenia were known, the role of SGLT1 remained less clear. The present study investigated the possible effect of SGLT1 inhibition on these conditions and explored potential mediators. Methods A two‐sample Mendelian randomization (MR) analysis was performed to assess the effect of SGLT1 inhibition on frailty index (FI) and low grip strength in individuals aged 60 years and older using both the FNIH and EWGSOP criteria. Subsequently, a two‐step MR analysis was conducted to investigate the mediating role of insulin resistance phenotype and identify potential mediators of the effect of SGLT1 inhibition on the FI and low grip strength from 1558 plasma proteins and 1352 metabolites. Results Genetically predicted SGLT1 inhibition was associated with decreased FI ( β : −0.290 [95% CI: −0.399, −0.181]) and reduced risk of low grip strength in individuals aged 60 years and older under both FNIH ( β : −0.796 [95% CI: −1.216, −0.376]) and EWGSOP criteria ( β : −0.287 [95% CI: −0.532, −0.041]). The two‐step MR analysis demonstrated the role of insulin resistance phenotype in mediating SGTL1 inhibition on alleviating frailty (mediation proportion = 19.56% [95% CI: 8.42%, 30.70%]). After screening, 24 proteins and 16 metabolites were identified as mediators of the impact of SGLT1 inhibition on FI. Additionally, 13 proteins and 16 metabolites were found to mediate the effect of SGLT1 inhibition on low grip strength according to FNIH criteria while 22 proteins and 6 metabolites were shown to mediate the impact of SGLT1 inhibition on low grip strength under EWGSOP criteria. Conclusions SGLT1 inhibition potentially mitigated frailty and sarcopenia through several biological mediators, shedding new light for therapeutic intervention.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
李园长完成签到,获得积分10
1秒前
angelfern发布了新的文献求助10
1秒前
科研助理795的应助被温暖妙彤采纳,获得10
1秒前
1秒前
2秒前
GDD完成签到,获得积分10
2秒前
window1000发布了新的文献求助10
2秒前
3秒前
2758543477完成签到,获得积分10
3秒前
3秒前
burning发布了新的文献求助10
4秒前
6秒前
可爱的函函的应助被hang航采纳,获得10
6秒前
xiaobai发布了新的文献求助10
8秒前
正直衫发布了新的文献求助30
8秒前
cc完成签到,获得积分10
8秒前
疯狂输出完成签到 ,获得积分10
8秒前
秦千默完成签到,获得积分10
9秒前
ty完成签到 ,获得积分10
9秒前
wxy完成签到,获得积分10
9秒前
科研通AI6.4的应助被占翠萱采纳,获得10
10秒前
shuangma完成签到,获得积分10
10秒前
可爱的函函的应助被淡淡白羊采纳,获得10
10秒前
11秒前
11秒前
12秒前
小兔兔猎魊完成签到,获得积分10
13秒前
14秒前
14秒前
Wanderer完成签到,获得积分10
14秒前
14秒前
14秒前
orixero的应助被吴彦祖采纳,获得10
15秒前
星辰大海的应助被XT采纳,获得10
16秒前
16秒前
愉快惜寒完成签到,获得积分10
17秒前
17秒前
胡图图完成签到,获得积分10
17秒前
田様的应助被CUCUMBER采纳,获得10
17秒前
单身的伟帮完成签到,获得积分10
18秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Energie-Contracting 1500
Klimaschutzrecht durch den Energiesektor im Mehrebenensystem – Ein Rechtsvergleich 1000
Oncology Clinical Trials: Successful Design, Conduct, and Analysis, Second Edition 800
Comprehensive Heterocyclic Chemistry IV 400
Qualitative Methodologies in Tourism Studies: Disrupting and Co-creating Critical Research 350
Représentation chimique de la structure des kérogènes et des asphaltènes en fonction de leur origine et de leur degré d'évolution 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 工程类 有机化学 化学工程 生物化学 物理 复合材料 内科学 催化作用 光电子学 人工智能 细胞生物学 无机化学 物理化学 数学
热门帖子
关注 科研通微信公众号,转发送积分 8051691
求助须知:如何正确求助?哪些是违规求助? 9479625
关于积分的说明 21298839
捐赠科研通 7620027
什么是DOI,文献DOI怎么找? 3393536
关于科研通互助平台的介绍 2524818
邀请新用户注册赠送积分活动 2431558