Equine Metabolic Syndrome (EMS) is characterized by abnormalities in insulin regulation, increased adiposity and laminitis, and has several similarities to human metabolic syndrome. A large amount of environmental variability in the EMS phenotype is not explained by commonly measured factors (diet, exercise, and season), suggesting that other environmental factors play a role in EMS development. Endocrine disrupting chemicals (EDCs) are associated with metabolic syndrome and other endocrine abnormalities in humans. This led us to hypothesize that EDCs are detectable in horse plasma and play a role in the pathophysiology of EMS. EDCs acting through the aryl hydrocarbon and estrogen receptors, were measured in plasma of 301 horses from 32 farms. The median (range) TEQ (2,3,7,8-TCDD equivalent) and EEQ (17β-estradiol equivalent) were 19.29 pg/g (0.59–536.36) and 10.50 pg/ml (4.35–15000.00), respectively. TEQ was negatively associated with plasma fat extracted and batch analyzed. EEQ was positively associated with pregnancy and batch analyzed, and negatively associated with being male and superfund score ≤100 miles of the farm. Of particular interest, serum glucose and insulin, glucose and insulin post oral sugar challenge, and leptin concentrations were associated with EEQ, and serum triglyceride concentration was associated with TEQ. Overall, we demonstrated that EDCs are present in the plasma of horses and may explain some of the environmental variability in measured EMS phenotypes. This is the first example of EDCs being associated with clinical disease phenotype components in domestic animals.
Bibliographical noteFunding Information:
This work was supported by: USDA NIFA-AFRI Project 2009-55205-05254 : Integrated Research and Extension Program for Equine Metabolic Syndrome and Shivers and the Morris Animal Foundation D14EQ-033 : Understanding Genetic Risk Factors for Metabolic Syndrome and D15EQ-029 : Role of endocrine disrupting chemicals in equine metabolic syndrome. Salary support for SA Durward-Akhurst was provided by an American College of Veterinary Internal Medicine Foundation fellowship, and by a T32 Institutional Training Grant in Comparative Medicine and Pathology ( 5T320D010993-12 ). The authors acknowledge the Minnesota Supercomputing Institute (MSI) at the University of Minnesota for providing resources that contributed to the research results reported within this paper. URL: http://www.msi.umn.edu . Appendix A
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