Send to

Choose Destination
Am J Obstet Gynecol. 2011 Jun;204(6):479-87. doi: 10.1016/j.ajog.2010.11.039. Epub 2011 Feb 2.

Is it time to revisit the Pedersen hypothesis in the face of the obesity epidemic?

Author information

Department of Reproductive Biology, Case Western Reserve University at MetroHealth Medical Center, Cleveland, OH, USA.


The Pedersen hypothesis was formulated more than 50 years ago. Jorgen Pedersen primarily cared for women with type 1 diabetes. He suggested that fetal overgrowth was related to increased transplacental transfer of glucose, stimulating the release of insulin by the fetal beta cell and subsequent macrosomia. Optimal maternal glucose control decreased perinatal mortality and morbidity. However, over the ensuing decades, there have been increases in maternal obesity and subsequently gestational diabetes mellitus (GDM) and type 2 diabetes. The underlying pathophysiology of type 1 and GDM/type 2 diabetes are fundamentally different, type 1 diabetes being primarily a disorder of beta cell failure and type 2 diabetes/GDM including both insulin resistance and beta cell dysfunction. As such the metabolic milieu in which the developing fetus is exposed may be quite different in type 1 diabetes and obesity. In this review we examine the metabolic environment of obese diabetic women and lipid metabolism affecting fetal adiposity. The importance of understanding these issues relates to the increasing trends of obesity worldwide with perinatal programming of metabolic dysfunction in the offspring.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center