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Animal genetics2020; 51(4); 607-610; doi: 10.1111/age.12952

Assessment of the FAM174A 11G allele as a risk allele for equine metabolic syndrome.

Abstract: An 11G nucleotide repeat in the 3' UTR of FAM174A was recently postulated as a risk allele with a dominant mode of inheritance for equine metabolic syndrome (EMS) and laminitis status in Arabian horses. The objective of this project was to evaluate this hypothesis in a large and diverse across-breed population. A total of 301 ponies, 292 Morgans, 64 Arabians, 49 Tennessee Walking Horses and 59 Quarter Horses were genotyped for six observed G repeat alleles in the FAM174A 3' UTR. Phenotype data included laminitis status, baseline insulin, glucose, non-esterified fatty acids, triglycerides, adiponectin, leptin, ACTH, insulin and glucose post oral sugar test, and two proxies for insulin resistance. The 11G allele frequencies were 18.8, 6.9, 1.8, 0.2 and 0.0% in the Arabians, Tennessee Walkers, ponies, Morgans and Quarter Horses respectively. Association analyses between FAM174A genotype and EMS phenotypes, and between allele count and EMS phenotypes, identified no statistically significant associations. When a dominant effect for the 11G allele was evaluated, a statistically significant association with adiponectin levels was identified in the ponies, and pairwise comparisons revealed that the estimated marginal means were higher in ponies with the 11G allele vs. alternative alleles (i.e. the allele had a protective effect). In conclusion, our data do not support the FAM174A 11G allele as a risk allele for EMS in our studied breeds.
© 2020 Stichting International Foundation for Animal Genetics.
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Publication Date: 2020-05-15 PubMed ID: 32412131DOI: 10.1111/age.12952Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research investigates whether the presence of the FAM174A 11G allele, a particular variant of DNA, increases the risk of metabolic syndrome in horses of various breeds. They found no significant association between the allele and metabolic syndrome, contradicting previous studies which suggested it to be a risk factor, particularly in Arabian horses.

Study Design and Sample

  • The researchers conducted the study across a large and diverse population of horses, including 301 ponies, 292 Morgans, 64 Arabians, 49 Tennessee Walking Horses, and 59 Quarter Horses.
  • They genotyped these horses for six different variants of the G repeat alleles found within the FAM174A 3′ UTR, the specific DNA sequence they were investigating.
  • The phenotype data they collected included a variety of factors relating to metabolic syndrome, such as laminitis status, baseline insulin, glucose, non-esterified fatty acids, triglycerides, adiponectin, leptin, ACTH, insulin and glucose post oral sugar test, and two markers for insulin resistance.

Data Results

  • The researchers found that the frequency of the 11G allele varied significantly among the different breeds, with the highest frequency in Arabian horses (18.8%) and no occurrences in Quarter Horses.
  • However, when testing for an association between the presence of the FAM174A genotype and the various metabolic syndrome phenotypes in these horses, they found no statistically significant associations.

Outcomes and Conclusion

  • In contrast to previous research, they did not find evidence to support the idea that the FAM174A 11G allele is a risk factor for equine metabolic syndrome.
  • The only statistically significant association found during the research was with adiponectin levels in ponies, suggesting that the presence of the 11G allele might have a protective effect against metabolic syndrome in this specific breed.
  • Overall, the research findings indicate that further investigation is needed to clarify the genetic factors influencing equine metabolic syndrome.

Cite This Article

APA
Roy MM, Norton EM, Rendahl AK, Schultz NE, McFarlane D, Geor RJ, Mickelson JR, McCue ME. (2020). Assessment of the FAM174A 11G allele as a risk allele for equine metabolic syndrome. Anim Genet, 51(4), 607-610. https://doi.org/10.1111/age.12952

Publication

Animal genetics
ISSN: 1365-2052
NlmUniqueID: 8605704
Country: England
Language: English
Volume: 51
Issue: 4
Pages: 607-610

Researcher Affiliations

Roy, M M
  • Veterinary Population Medicine Department, University of Minnesota, 225 Veterinary Medical Center, 1365 Gortner Ave, St Paul, MN, USA.
Norton, E M
  • Veterinary Population Medicine Department, University of Minnesota, 225 Veterinary Medical Center, 1365 Gortner Ave, St Paul, MN, USA.
Rendahl, A K
  • Veterinary and Biomedical Sciences Department, University of Minnesota, 295 An Sci Vet Med, 1988 Fitch Ave, St Paul, MN, 55108, USA.
Schultz, N E
  • Veterinary Population Medicine Department, University of Minnesota, 225 Veterinary Medical Center, 1365 Gortner Ave, St Paul, MN, USA.
McFarlane, D
  • Department of Physiological Sciences, Oklahoma State University, 264 McElroy Hall, Stillwater, OK, 74078, USA.
Geor, R J
  • College of Sciences, Massey University, B2.13, Science Tower B, Tennent Drive, Palmerston North, New Zealand.
Mickelson, J R
  • Veterinary and Biomedical Sciences Department, University of Minnesota, 295 An Sci Vet Med, 1988 Fitch Ave, St Paul, MN, 55108, USA.
McCue, M E
  • Veterinary Population Medicine Department, University of Minnesota, 225 Veterinary Medical Center, 1365 Gortner Ave, St Paul, MN, USA.

MeSH Terms

  • Alleles
  • Animals
  • Female
  • Foot Diseases / genetics
  • Foot Diseases / veterinary
  • Horse Diseases / genetics
  • Horses
  • Male
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / veterinary
  • Risk Factors

Grant Funding

  • D17EQ-019 / Morris Animal Foundation
  • D17EQ-402 / Morris Animal Foundation Doctoral Fellowship

References

This article includes 15 references
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Citations

This article has been cited 1 times.
  1. Wallis N, Raffan E. The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals. Genes (Basel) 2020 Nov 20;11(11).
    doi: 10.3390/genes11111378pubmed: 33233816google scholar: lookup
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