Relationship between liver and cardiometabolic health in type 1 diabetes.

IF 3.9 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM Frontiers in Endocrinology Pub Date : 2024-11-13 eCollection Date: 2024-01-01 DOI:10.3389/fendo.2024.1505430
Emir Tas, Bach-Mai Katherine Vu, Brenda Mendizabal, Ingrid Libman, Radhika Muzumdar
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Abstract

Introduction: Type 1 diabetes (T1D) is a chronic condition marked by insulin deficiency and hyperglycemia, with an increasing global incidence, particularly among children. Despite improvements in diabetes management, individuals with T1D continue to experience higher rates of cardiovascular disease (CVD), the leading cause of mortality in this population. Traditional CVD risk factors such as dyslipidemia and poor glycemic control are insufficient to fully explain the elevated risk in T1D, prompting further investigation into additional factors. Emerging evidence suggests that metabolic dysfunction-associated steatotic liver disease (MASLD) plays a critical role in this heightened CVD risk.

Objective: This narrative review aims to explore the relationship between MASLD and CVD in individuals with T1D. The review focuses on the prevalence of MASLD, its contributing risk factors, and the potential impact of liver dysfunction on cardiovascular outcomes in this population.

Methods: A review of existing literature was conducted, focusing on observational studies, cohort studies, and meta-analyses that investigate the prevalence of MASLD in T1D populations and its association with CVD. The review also examines the physiological mechanisms linking MASLD and CVD, including insulin resistance, systemic inflammation, and hepatic dyslipidemia. Key studies were evaluated to identify patterns in MASLD prevalence based on diagnostic modalities and to assess the independent contribution of MASLD to cardiovascular risk in T1D patients.

Conclusion: MASLD is increasingly recognized as a significant contributor to CVD in individuals with T1D, particularly in those with shared risk factors like obesity and insulin resistance. Evidence suggests that MASLD exacerbates hepatic and systemic metabolic dysfunction, increasing CVD risk through mechanisms such as chronic inflammation and atherogenic lipid profiles. Routine liver health assessments and tailored management strategies targeting MASLD should be incorporated into clinical care for individuals with T1D to mitigate long-term cardiovascular complications.

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1 型糖尿病患者肝脏与心脏代谢健康之间的关系。
简介1 型糖尿病(T1D)是一种以胰岛素缺乏和高血糖为特征的慢性疾病,全球发病率不断上升,尤其是在儿童中。尽管糖尿病管理有所改善,但 T1D 患者罹患心血管疾病(CVD)的比例仍然较高,而心血管疾病是导致该人群死亡的主要原因。血脂异常和血糖控制不佳等传统心血管疾病风险因素不足以完全解释 T1D 患者风险升高的原因,这促使人们进一步研究其他因素。新出现的证据表明,代谢功能障碍相关性脂肪性肝病(MASLD)在心血管疾病风险升高的过程中起着至关重要的作用:本叙述性综述旨在探讨 T1D 患者的代谢功能障碍相关性脂肪性肝病与心血管疾病之间的关系。综述的重点是 MASLD 的患病率、其诱发风险因素以及肝功能异常对该人群心血管疾病预后的潜在影响:对现有文献进行了综述,重点研究了T1D人群中MASLD的患病率及其与心血管疾病相关的观察性研究、队列研究和荟萃分析。综述还探讨了 MASLD 与心血管疾病相关的生理机制,包括胰岛素抵抗、全身炎症和肝脏血脂异常。对主要研究进行了评估,以确定基于诊断模式的MASLD患病率模式,并评估MASLD对T1D患者心血管风险的独立贡献:结论:人们日益认识到,MASLD是导致T1D患者心血管疾病的重要因素,尤其是在具有肥胖和胰岛素抵抗等共同风险因素的患者中。有证据表明,MASLD 会加剧肝脏和全身代谢功能障碍,通过慢性炎症和致动脉粥样硬化血脂等机制增加心血管疾病风险。应将常规肝脏健康评估和针对 MASLD 的定制管理策略纳入 T1D 患者的临床护理中,以减轻长期心血管并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Frontiers in Endocrinology
Frontiers in Endocrinology Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
5.70
自引率
9.60%
发文量
3023
审稿时长
14 weeks
期刊介绍: Frontiers in Endocrinology is a field journal of the "Frontiers in" journal series. In today’s world, endocrinology is becoming increasingly important as it underlies many of the challenges societies face - from obesity and diabetes to reproduction, population control and aging. Endocrinology covers a broad field from basic molecular and cellular communication through to clinical care and some of the most crucial public health issues. The journal, thus, welcomes outstanding contributions in any domain of endocrinology. Frontiers in Endocrinology publishes articles on the most outstanding discoveries across a wide research spectrum of Endocrinology. The mission of Frontiers in Endocrinology is to bring all relevant Endocrinology areas together on a single platform.
期刊最新文献
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