Maternal Serum Prolactin and Prediction of Postpartum β-Cell Function and Risk of Prediabetes/Diabetes.

Abstract

The insulin resistance of mid- to late pregnancy poses a physiologic stress test for the pancreatic β-cells, which must respond by markedly increasing their secretion of insulin. This response is achieved through an expansion of β-cell mass induced by the hormones prolactin and human placental lactogen (HPL). Conversely, the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has recently emerged as a negative regulator of β-cell function in pregnancy. Given their respective roles in the β-cell response to the stress test of gestation, we hypothesized that antepartum prolactin, HPL, and CMPF may relate to a woman's underlying glucoregulatory physiology and hence to her metabolic status after pregnancy.