Six of the seven SNPs are in metabolic genes, according to a study in American Journal of Human Genetics.

Two studies provide evidence that differences in blood levels of C reactive protein (CRP), a marker of cardiac events, stem in part from genetic variations in known metabolic genes.

Paul Ridker, M.D., of Harvard Medical School led a team that conducted a genome-wide association study among 6,345 apparently healthy women participating in the Women’s Genome Health Study. The study turned up seven sites that were significantly associated with CRP.

Of these seven loci, six were directly involved in metabolic syndrome, insulin resistance, insulin-producing beta-cell function, weight homeostasis, and/or premature atherothrombosis. Two genes are suspected to be associated with maturity-onset diabetes of the young, the Harvard scientists report. These genes are also responsible for glucokinase regulatory protein (GCKR), previously linked to triglyceride and glucose levels, and hepatic nuclear factor-1A (HNF1A).

The team also uncovered links between CRP levels and the inflammatory cytokine known as interleukin-6 as well as a site in or near the gene encoding leptin, a fat-produced hormone that regulates appetite and metabolism.

A second University of Washington led report of two additional genetic association studies from the Pharmacogenomics and Risk of Cardiovascular Disease Study and the Cardiovascular Health Study provided independent and confirmatory evidence for an association between common variants of HNF1A and CRP concentrations. Both studies also found links between blood CRP levels and the CRP gene itself in addition to the apolipoprotein E gene, consistent with earlier reports.

Both findings will be reported in the May  issue of the American Journal of Human Genetics.

Previous articleInvestigators Illuminate Mechanism for Controlling Cell Growth in Response to Energy Stress
Next articleScientists Characterize Protein Involved in Protecting Malaria Parasite during Infection