Evaluation of Circulating Determinants of Beta-Cell Function in Women With and Without Gestational Diabetes

Gestational diabetes (GDM) arises in women in whom there is insufficient β-cell compensation for the insulin resistance of late pregnancy. The mechanisms underlying both normal antepartum β-cell adaptation and its aberrancy in GDM are unclear. Preclinical studies have suggested that the hormones prolactin and human placental lactogen (HPL) may stimulate β-cell mass, whereas the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has recently emerged as a potential negative regulator of β-cell function. However, there has been limited study of these factors in humans.