Summary Background Equine metabolic syndrome ( EMS ) is a complex clinical disorder with both environmental and genetic factors contributing to EMS phenotypes. Estimates of heritability determine the proportion of variation in a trait that is attributable to genetics. Objectives To provide heritability estimates for nine metabolic traits associated with EMS in two high‐risk breeds. Study design Retrospective cohort study. Methods High‐density single‐nucleotide polymorphism ( SNP ) genotype data was used to estimate the heritability (h 2 SNP ) of nine metabolic traits relevant to EMS in a cohort of 264 Welsh ponies and 286 Morgan horses. Traits included measurements of insulin, glucose, non‐esterified fatty acids ( NEFA ), triglycerides, leptin, adiponectin, ACTH , and glucose ( GLU ‐ OST ) and insulin ( INS ‐ OST ) following an oral sugar challenge. Results In Welsh ponies, seven of the nine traits had statistically significant h 2 SNP estimates that were considered moderately to highly heritable (h 2 SNP >0.20) including: triglycerides (0.313; s.e. = 0.146), glucose (0.408; s.e. = 0.135), NEFA (0.434; s.e. = 0.136), INS ‐ OST (0.440; s.e. = 0.148), adiponectin (0.488; s.e. = 0.143), leptin (0.554; s.e. = 0.132) and insulin (0.808; s.e. = 0.108). In Morgans, six of the nine traits had statistically significant h 2 SNP estimates that were also determined to be moderately to highly heritable including: INS ‐ OST (0.359; s.e. = 0.185), leptin (0.486; s.e. = 0.177), GLU ‐ OST (0.566 s.e. = 0.175), insulin (0.592; s.e. = 0.195), NEFA (0.684; s.e. = 0.164), and adiponectin (0.913; s.e. = 0.181). Main limitations Insufficient population size may have limited power to obtain statistically significant h 2 SNP estimates for ACTH (both breeds), glucose and triglycerides in Morgans and GLU ‐ OST in Welsh ponies. Conclusions This study provides the first concrete evidence of a genetic contribution to key phenotypes associated with EMS . Eight of these nine traits had moderate to high h 2 SNP estimates in this cohort. These data demonstrate that continued research for identification of the genetic risk factors for EMS phenotypes within and across breeds is warranted.