Genes influence risk of gestational diabetes, but not eventual type 2 diabetes

By Reuters Staff

NEW YORK (Reuters Health) - Genetic makeup appears to influence the risk of developing gestational diabetes, but not the risk of progression to type 2 diabetes, according to results from the Diabetes Prevention Program (DPP) trial.

The DPP showed that women with prediabetes and prior gestational diabetes (GDM) were more likely than women without prior GDM to develop diabetes. Moreover, intensive lifestyle intervention prevented progression to diabetes in both groups, whereas metformin was more effective in women with a history of GDM.

Dr. Shannon D. Sullivan from MedStar Washington Hospital Center in Washington, D.C., and colleagues in the DPP Research Group wondered whether genetic variability could account for these differences. They compared beta-cell function between 281 women with GDM and 1,102 women without GDM and examined the utility of a 34-locus genetic risk score (GRS) in predicting progression to diabetes and response to intervention (placebo, metformin, or intensive lifestyle intervention).

At baseline and one year later, beta-cell function (as measured by the insulinogenic index) was significantly decreased in GDM women versus non-GDM women.

After adjustment for ethnicity and age, each unit increase in the GRS was associated with a 5% increase in the odds of GDM, according to the report, online November 22 in Diabetes Care.

The association between GRS and GDM disappeared after adjustment for waist circumference.

GRS did not predict progression to diabetes in women with or without GDM after adjustment for ethnicity, age, and treatment arm.

After excluding the four single nucleotide polymorphisms (SNPs) primarily associated with insulin resistance, none of the 30 remaining SNPs independently predicted insulin sensitivity in women with GDM compared with women without GDM.

"These data suggest a diabetes-associated GRS is associated with development of GDM, and may characterize women at risk for development of diabetes due to beta-cell dysfunction," the researchers conclude.

The authors stop short of discussing whether these findings have implications for the management of women with GDM and beta-cell dysfunction.

Dr. Sullivan did not respond to a request for comments.

SOURCE: http://bit.ly/1f3bhXa

Diabetes Care 2013.

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