A placental protein (11β-HSD2) may protect against future development of diabetes

What is it about?

Type-2 diabetes mellitus (T2DM) is a major public health burden. T2DM is often developed after the body becomes “insulin resistant” – a condition that prevents tissues using insulin to remove glucose from the blood. A number of studies have found that the development of type 2 diabetes may have its roots in early life, but the specific factors contributing to disease development remain unclear. Our research suggests that a placental protein called placental 11 β-hydroxysteroid dehydrogenase 2 (11β-HSD2) may protect against the development of T2DM in early life. 11β-HSD2 is an enzyme that converts active glucocorticoid – cortisol to its biologically inactive form, cortisone. Cortisol is released in large amounts in response to various stresses in pregnant women. The presence of 11β-HSD2 in the placenta provides a barrier to reduce exposure of the fetus to the mothers circulating cortisol, hence cortisol concentrations in the unborn baby are much lower than in the mother. Our study of 246 mother-baby pairs has shown that the higher the placental 11β-HSD2 level, the lower the insulin resistance in infants at 1 year of age, suggesting that increased placental 11β-HSD2 may convey longer term protection against the development of type-2 diabetes in the early years of life.

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Why is it important?

This finding points to a new molecular target (placental 11β-HSD2) for developing effective early life interventions to safeguard against the development of type 2 diabetes.

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