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东亚人群中的代谢性疾病。

Metabolic diseases in the East Asian populations.

作者信息

Sun Zhonghan, Zheng Yan

机构信息

State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Zhongshan Hospital, Fudan University, Shanghai, China.

Department of Nutrition and Food Hygiene, School of Public Health, Institute of Nutrition, Fudan University, Shanghai, China.

出版信息

Nat Rev Gastroenterol Hepatol. 2025 Apr 8. doi: 10.1038/s41575-025-01058-8.

DOI:10.1038/s41575-025-01058-8
PMID:40200111
Abstract

East Asian populations, which account for approximately 20% of the global population, have become central to the worldwide rise of metabolic diseases over the past few decades. The prevalence of metabolic disorders, including type 2 diabetes mellitus, hypertension and metabolic dysfunction-associated steatotic liver disease, has escalated sharply, contributing to a substantial burden of complications such as cardiovascular disease, chronic kidney disease, cancer and increased mortality. This concerning trend is primarily driven by a combination of genetic predisposition, unique fat distribution patterns and rapidly changing lifestyle factors, including urbanization and the adoption of Westernized dietary habits. Current advances in genomics, proteomics, metabolomics and microbiome research have provided new insights into the biological mechanisms that might contribute to the heightened susceptibility of East Asian populations to metabolic diseases. This Review synthesizes epidemiological data, risk factors and biomarkers to provide an overview of how metabolic diseases are reshaping public health in East Asia and offers insights into biological and societal drivers to guide effective, region-specific strategies.

摘要

东亚人口约占全球人口的20%,在过去几十年里,已成为全球代谢性疾病发病率上升的核心因素。包括2型糖尿病、高血压和代谢功能障碍相关脂肪性肝病在内的代谢紊乱患病率急剧上升,导致心血管疾病、慢性肾脏病、癌症等并发症负担沉重,并增加了死亡率。这一令人担忧的趋势主要是由遗传易感性、独特的脂肪分布模式以及包括城市化和采用西化饮食习惯在内的快速变化的生活方式因素共同驱动的。基因组学、蛋白质组学、代谢组学和微生物组研究的最新进展,为可能导致东亚人群对代谢性疾病易感性增加的生物学机制提供了新的见解。本综述综合了流行病学数据、风险因素和生物标志物,概述了代谢性疾病如何重塑东亚地区的公共卫生,并深入探讨了生物学和社会驱动因素,以指导有效的、针对该地区的策略。

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本文引用的文献

1
Global burden of metabolic dysfunction-associated steatotic liver disease, 2010 to 2021.2010年至2021年代谢功能障碍相关脂肪性肝病的全球负担
JHEP Rep. 2024 Nov 14;7(3):101271. doi: 10.1016/j.jhepr.2024.101271. eCollection 2025 Mar.
2
Biobanking with genetics shapes precision medicine and global health.带有遗传学的生物样本库塑造了精准医学和全球健康。
Nat Rev Genet. 2025 Mar;26(3):191-202. doi: 10.1038/s41576-024-00794-y. Epub 2024 Nov 20.
3
Non-invasive lipid panel of MASLD fibrosis transition underscores the role of lipoprotein sulfatides in hepatic immunomodulation.
非侵入性代谢相关脂肪性肝病(MASLD)纤维化转变的血脂谱强调了脂蛋白硫脂在肝脏免疫调节中的作用。
Cell Metab. 2025 Jan 7;37(1):69-86.e7. doi: 10.1016/j.cmet.2024.09.009. Epub 2024 Nov 4.
4
A blood-based biomarker panel for non-invasive diagnosis of metabolic dysfunction-associated steatohepatitis.用于非侵入性诊断代谢功能障碍相关脂肪性肝炎的血液生物标志物组合
Cell Metab. 2025 Jan 7;37(1):59-68.e3. doi: 10.1016/j.cmet.2024.10.008. Epub 2024 Nov 4.
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Effects of healthy low-carbohydrate diet and time-restricted eating on weight and gut microbiome in adults with overweight or obesity: Feeding RCT.健康低碳水化合物饮食和限时进食对超重或肥胖成年人体重和肠道微生物组的影响:喂养 RCT。
Cell Rep Med. 2024 Nov 19;5(11):101801. doi: 10.1016/j.xcrm.2024.101801. Epub 2024 Oct 24.
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Metabolic syndrome.代谢综合征。
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Enteropancreatic hormone changes in caloric-restricted diet interventions associate with post-intervention weight maintenance.热量限制饮食干预与干预后体重维持相关的肠胰激素变化。
Clin Nutr. 2024 Dec;43(12):5-14. doi: 10.1016/j.clnu.2024.10.004. Epub 2024 Oct 5.
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A genome-wide association analysis reveals new pathogenic pathways in gout.全基因组关联分析揭示了痛风的新致病途径。
Nat Genet. 2024 Nov;56(11):2392-2406. doi: 10.1038/s41588-024-01921-5. Epub 2024 Oct 15.
9
Assessing the Hypertension Risk: A Deep Dive into Cereal Consumption and Cooking Methods-Insights from China.评估高血压风险:深入探讨谷物消费和烹饪方法——来自中国的见解。
Nutrients. 2024 Sep 8;16(17):3027. doi: 10.3390/nu16173027.
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Association Between Adherence to EAT-Lancet Diet and Risk of Hypertension: An 18-Year National Cohort Study in China.坚持EAT-柳叶刀饮食与高血压风险之间的关联:一项在中国进行的为期18年的全国队列研究。
J Am Nutr Assoc. 2025 Jan;44(1):40-49. doi: 10.1080/27697061.2024.2399826. Epub 2024 Sep 5.