People diagnosed with type 2 diabetes (T2D) at a young age face (defined as T2D diagnosed before age 40 years) markedly higher lifelong risks of vascular and metabolic complications, yet the mechanisms driving this excess risk remain poorly understood. Ethnically diverse populations are also disproportionately affected by early and severe T2D, but the biological and contextual factors underlying these disparities are not well characterized. Large gaps persist in understanding how age at diagnosis interacts with ancestry, ethnicity, environment, and molecular pathways to shape long-term outcomes.
This project will function to characterize clinical, biological, and sociodemographic determinants of T2D across diverse populations and across ages at diagnosis.
Research Questions:
How do biological pathways, environmental exposures, and population-level factors differ across age at T2D diagnosis, and how do these patterns vary among ethnically diverse groups?
Do metabolomic signatures differ by age at T2D onset, and can these signatures help explain the disproportionate complication risk observed in young-onset T2D?
Objectives:
(1) Define metabolic, genetic, and clinical profiles across age of diagnosis;
(2) Examine T2D heterogeneity across diverse ancestral groups;
(3) Identify pathways and modifiable factors contributing to excess cardiometabolic risk; and
(4) Generate evidence to support precision prevention and management strategies.
We will evaluate plasma metabolomics to identify pathways distinguishing young-onset from later-onset T2D. Future directions may incorporate genetics, polygenic scores, longitudinal outcomes, environmental exposures, multimorbidity, and treatment patterns to understand how both ethnic differences and variations in age at diagnosis pose disparities in T2D pathogenesis.
