Skeletal muscle disorders as risk factors for type 2 diabetes

IF 3.6 3区 医学 Q2 CELL BIOLOGY Molecular and Cellular Endocrinology Pub Date : 2025-01-21 DOI:10.1016/j.mce.2025.112466
Eshwar R. Tammineni , Carlo Manno , Goldie Oza , Lourdes Figueroa
{"title":"Skeletal muscle disorders as risk factors for type 2 diabetes","authors":"Eshwar R. Tammineni ,&nbsp;Carlo Manno ,&nbsp;Goldie Oza ,&nbsp;Lourdes Figueroa","doi":"10.1016/j.mce.2025.112466","DOIUrl":null,"url":null,"abstract":"<div><div>The incidence and prevalence of muscular disorders and of type 2 diabetes (T2D) is increasing and both represent highly significant healthcare problems, both economically and compromising quality of life. Interestingly, skeletal muscle dysfunction and T2D share some commonalities including dysregulated glucose homeostasis, increased oxidative stress, dyslipidemia, and cytokine alterations. Several lines of evidence have hinted to a relationship between skeletal muscle dysfunction and T2D. For instance, T2D affects skeletal muscle morphology, functionality, and overall health through altered protein metabolism, impaired mitochondrial function, and ultimately cell viability. Conversely, humans suffering from myopathies and their experimental models demonstrated increased incidence of T2D through altered muscle glucose disposal function due to abnormal calcium homeostasis, compromised mitochondrial function, dyslipidemia, increased inflammatory cytokines and fiber size alterations and disproportions. Lifestyle modifications are essential for improving and maintaining mobility and metabolic health in individuals suffering from myopathies along with T2D. In this review, we updated current literature evidence on clinical incidence of T2D in inflammatory, mitochondrial, metabolic myopathies, and muscular dystrophies and further discussed the molecular basis of these skeletal muscle disorders leading to T2D.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"599 ","pages":"Article 112466"},"PeriodicalIF":3.6000,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0303720725000176","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The incidence and prevalence of muscular disorders and of type 2 diabetes (T2D) is increasing and both represent highly significant healthcare problems, both economically and compromising quality of life. Interestingly, skeletal muscle dysfunction and T2D share some commonalities including dysregulated glucose homeostasis, increased oxidative stress, dyslipidemia, and cytokine alterations. Several lines of evidence have hinted to a relationship between skeletal muscle dysfunction and T2D. For instance, T2D affects skeletal muscle morphology, functionality, and overall health through altered protein metabolism, impaired mitochondrial function, and ultimately cell viability. Conversely, humans suffering from myopathies and their experimental models demonstrated increased incidence of T2D through altered muscle glucose disposal function due to abnormal calcium homeostasis, compromised mitochondrial function, dyslipidemia, increased inflammatory cytokines and fiber size alterations and disproportions. Lifestyle modifications are essential for improving and maintaining mobility and metabolic health in individuals suffering from myopathies along with T2D. In this review, we updated current literature evidence on clinical incidence of T2D in inflammatory, mitochondrial, metabolic myopathies, and muscular dystrophies and further discussed the molecular basis of these skeletal muscle disorders leading to T2D.
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
骨骼肌疾病是2型糖尿病的危险因素。
肌肉疾病和2型糖尿病(T2D)的发病率和患病率正在增加,两者都是非常重要的医疗保健问题,既经济上又影响生活质量。有趣的是,骨骼肌功能障碍和T2D有一些共同之处,包括葡萄糖稳态失调、氧化应激增加、血脂异常和细胞因子改变。一些证据暗示了骨骼肌功能障碍和T2D之间的关系。例如,T2D通过改变蛋白质代谢、线粒体功能受损以及最终影响细胞活力来影响骨骼肌形态、功能和整体健康。相反,患有肌病的人及其实验模型表明,由于钙稳态异常、线粒体功能受损、血脂异常、炎症细胞因子增加、纤维大小改变和比例失调,肌肉葡萄糖处理功能发生改变,从而增加了T2D的发病率。生活方式的改变对于改善和维持肌病伴T2D患者的活动能力和代谢健康至关重要。在这篇综述中,我们更新了目前关于炎性、线粒体、代谢性肌病和肌肉萎缩症中T2D临床发病率的文献证据,并进一步讨论了导致T2D的这些骨骼肌疾病的分子基础。
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
Molecular and Cellular Endocrinology
Molecular and Cellular Endocrinology 医学-内分泌学与代谢
CiteScore
9.00
自引率
2.40%
发文量
174
审稿时长
42 days
期刊介绍: Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the genetic and biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
期刊最新文献
Editorial Board Developmental exposure to a mixture of propiconazole and glyphosate induces histopathological lesions in the prostate of postpubertal rats Integrative advances in endocrine oncology: From unique glimpses to familiar themes Toward intelligent hormonal diagnostics: Quantum dots reshaping endocrine disease detection EGR1 promotes ferroptosis in endometriosis through transcriptional activation of HMOX1
×
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:604180095
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