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PhD Seminar - Tahzeeb Fatima

Biochemistry Department, University of Otago

Gout and Metabolic Disease: Investigation of Potential Relationship in the New Zealand Population

Biochemistry Seminar Room 231
May. 30, 2017
  • 12:00

Hyperuricaemia, the presence of higher levels of serum urate, results from a compromise in the delicate balance between the production and excretion of urate primarily in the liver and the kidneys, respectively. Hyperuricaemia is a prerequisite for gout, a painful inflammatory arthritis. The symptoms of gout arise from the body’s immune response to monosodium urate crystals that accumulate in the synovial fluid of the joints. Hyperuricaemia and gout are complex traits. A number of genetic loci confer risk to develop hyperuricaemia. Genome-wide association studies (GWAS), an indispensable tool in population genetics, have identified at least twenty eight genomic loci that contain variants affecting serum urate concentration. Gene-environment interactions also play a significant role in this context. Exogenous factors such as the intake of purine-rich foods increase the frequency of gout flares. Population-specific genetic effects on gout are as evident, if not more, as for other complex phenotypes. The prevalence of gout is much higher in the New Zealand Polynesian population compared to other populations. Approximately 7% of New Zealand Māori and Pacific Island people and 3% of New Zealand Europeans are affected by gout.

The coexistence of metabolic conditions with gout, usually called gout-comorbidities, adds another level of complexity. However, not many studies have attempted to address the causal relationship between these traits. In fact, my research project was instigated as an attempt to study the causal associations between gout and its comorbidities and fill in some gap in the scientific literature. The research was, however, limited to three metabolic conditions/comorbidities of gout – imbalanced iron homeostasis, metabolic syndrome and disrupted lipid metabolism. My study reports a causal role of iron and ferritin in increasing serum urate concentration and the involvement of imbalanced iron homeostasis in hyperuricaemia. Positive genetic associations indicated that the genes involved in metabolic syndrome and lipid metabolism can potentially increase the risk for gout. Further, variants in these genes exhibit population-specific effects for the Polynesian and European ancestral groups in New Zealand.