James E. Haddow, MD, co-director of the Division of Medical Screening and Special Testing at Women & Infants Hospital, a Care New England hospital, and professor in the Department of Pathology and Laboratory Medicine at The Warren Alpert Medical School of Brown University; Geralyn M. Messerlian, PhD, director of the Division of Medical Screening and Special Testing and a professor in the Department of Pathology and Laboratory Medicine at the Alpert Medical School; Glenn E. Palomaki, PhD, associate director of the division and associate professor in the Department of Pathology and Laboratory Medicine at the Alpert Medical School, in collaboration with investigators in Dublin, New York, and Maine, have published their study “Free Thyroxine During Early Pregnancy and Risk for Gestational Diabetes” in the Public Library of Science (PLOS) ONE.
According to Dr. Haddow, their findings are the first to show that the well-known connection between obesity and gestational diabetes can be partially explained by altered thyroid hormone production. The thyroid gland itself functions normally among women with gestational diabetes. Altered thyroid hormone production takes place elsewhere in the body, where the inactive form of the hormone [thyroxine (T4)] is converted to the active form of the hormone [triiodothyronine (T3)].
Gestational diabetes mellitus (GDM) affects between three and 10 percent of pregnant women in the United States, depending on the nature of the population and how GDM is diagnosed. Women who are overweight or obese, older women, and some ethnic groups (particularly Asian women) are at particularly high risk.
The team identified obesity-induced deiodinase enzymes in the liver and muscles as the agent responsible for activating T3. Primary elements of this discovery emerged from analyses performed as an extension of a large observational study sponsored by the National Institutes of Health. Insights gathered from other published sources then supplemented the primary discovery.
“Previously, nobody has connected the dots of triiodothyronine (T3) being a factor in gestational diabetes,” said Dr. Haddow. “The publication describes our finding that higher caloric intake leading to obesity, can trigger an increase in the active form of thyroid hormone, thereby contributing to gestational diabetes.”
“At present, accumulation of fat in the liver and muscles associated with over-nutrition is the best understood cause of insulin-resistance and type 2 diabetes,” said Dr. Haddow. “Our discovery identifies T3 as an additional causal agent, again driven by calories. While there is no immediate, obvious solution to modify the T3 hormonal balance associated with gestational diabetes other than weight reduction, our discovery is certainly a next step in allowing research questions to be designed aimed at improving management.”
For more information on the Women & Infants Division of Medical Screening and Special Testing visit http://www.womenandinfants.org/services/medical-screening/.
About PLOS ONE
The world’s first multidisciplinary Open Access journal, PLOS ONE accepts scientifically rigorous research, regardless of novelty. PLOS ONE’s broad scope provides a platform to publish primary research, including interdisciplinary and replication studies as well as negative results. The journal’s publication criteria are based on high ethical standards and the rigor of the methodology and conclusions reported.
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