Genetic interaction effects reveal lipid-metabolic and inflammatory pathways underlying common metabolic disease risks.

ABSTRACT:

Background

Common metabolic diseases, including type 2 diabetes, coronary artery disease, and hypertension, arise from disruptions of the body's metabolic homeostasis, with relatively strong contributions from genetic risk factors and substantial comorbidity with obesity. Although genome-wide association studies have revealed many genomic loci robustly associated with these diseases, biological interpretation of such association is challenging because of the difficulty in mapping single-nucleotide polymorphisms (SNPs) onto the underlying causal genes and pathways. Furthermore, common diseases are typically highly polygenic, and conventional single variant-based association testing does not adequately capture potentially important large-scale interaction effects between multiple gen

SUBMITTER: Woo HJ 

PROVIDER: S-EPMC6011398 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature