Metabolomics of Type 1 and Type 2 Diabetes: Insights into Risk Prediction and Mechanisms

被引:16
作者
Izundegui, Daniel Gonzalez [1 ]
Nayor, Matthew [2 ,3 ,4 ]
机构
[1] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Med, Sect Cardiol, 72 E Concord St,Suite L-516, Boston, MA 02118 USA
[3] Boston Univ, Sch Med, Dept Med, Sect Prevent Med, 72 E Concord St,Suite L-516, Boston, MA 02118 USA
[4] Boston Univ, Sch Med, Dept Med, Sect Epidemiol, 72 E Concord St,Suite L-516, Boston, MA 02118 USA
关键词
Metabolomics; Type; 1; diabetes; 2; Risk prediction; ASYMMETRIC DIMETHYLARGININE ADMA; CHAIN AMINO-ACIDS; INSULIN-RESISTANCE; CARDIOVASCULAR-DISEASE; METABOLITE PROFILES; BETA-OXIDATION; GLUCOSE; DYSFUNCTION; PROGRESSION; RETINOPATHY;
D O I
10.1007/s11892-022-01449-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of Review Metabolomics enables rapid interrogation of widespread metabolic processes making it well suited for studying diabetes. Here, we review the current status of metabolomic investigation in diabetes, highlighting its applications for improving risk prediction and mechanistic understanding. Recent findings Findings of metabolite associations with type 2 diabetes risk have confirmed experimental observations (e.g., branched-chain amino acids) and also pinpointed novel pathways of diabetes risk (e.g., dimethylguanidino valeric acid). In type 1 diabetes, abnormal metabolite patterns are observed prior to the development of autoantibodies and hyperglycemia. Diabetes complications display specific metabolite signatures that are distinct from the metabolic derangements of diabetes and differ across vascular beds. Lastly, metabolites respond acutely to pharmacologic treatment, providing opportunities to understand inter-individual treatment responses. Metabolomic studies have elucidated biological mechanisms underlying diabetes development, complications, and therapeutic response. While not yet ready for clinical translation, metabolomics is a powerful and promising precision medicine tool.
引用
收藏
页码:65 / 76
页数:12
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