ABSTRACT
Type 1 diabetes is an autoimmune disease characterized by absolute insulin defi ciency. Hyperglycemia and its associated metabolic dysfunctions including endothelial damage could aff ect both macro-and microvasculature, leading to the development and progression of complications in patients with type 1 diabetes. Increased levels of soluble forms of various cell adhesion molecules, such as ICAM-1, VCAM-1, and ELAM-1 (endothelial leukocyte adhesion molecule 1), have been associated with type 1 diabetic patients with microangiopathy (Nowak et al. 2008). First, circulating levels of ICAM-1 appeared to be consistently associated with the presence or progression of retinopathy in patients with type 1 diabetes (Blann and Lip 1998). Th e association between ICAM-1 and type 1 diabetes has been supported by the fi ndings from in vitro and in vivo data showing that ICAM-1 may regulate immune activation and infl ammatory response (Blann and Lip 1998). Second, some but not all studies have reported elevated levels of E-selectin in patients with type 1 diabetes with microangiopathy. Due to sparse data, it remains controversial whether E-selectin is a reliable marker for type 1 diabetes with or without complications. Th ird, inferences from available studies regarding the link of soluble VCAM-1 to type 1 diabetes were hindered by their small sample sizes and inconsistent results. Finally, it is worth mentioning that endothelial damage may be involved in the pathogenesis of type 1 diabetes, but prospective data are lacking. Gestational diabetes mellitus (GDM) was defi ned as glucose intolerance with onset or fi rst recognition during pregnancy (Buchanan and Xiang 2005). Most women who developed GDM had underlying insulin resistance to which the insulin resistance of pregnancy was partly additive (Buchanan and Xiang 2005). Th ere is no evidence suggesting that the formation of placental vascular bed causes alterations in endothelial function as refl ected by the shedding of soluble adhesion molecules into maternal circulation during normal pregnancy (Chaiworapongsa et al. 2002). However, there is some evidence indicating a more signifi cant rise in circulating levels of endothelial cell adhesion molecules in pregnant women with GDM as compared with healthy pregnant women. For instance, E-selectin and VCAM-1 levels have been observed to be signifi cantly higher in pregnant women with GDM than in normal pregnant controls in some but not all studies (Kautzky-Willer et al. 1997, Lawrence et al. 2002, Telejko et al. 2009). Some studies have reported that levels of ICAM-1 and VCAM-1 among GDM women were similar to those in healthy pregnant women, although these endothelial markers were slightly lower in healthy pregnant women than in GDM women (KautzkyWiller et al. 1997). Overall, fi ndings from sparse and inclusive data indicated that endothelial dysfunction as refl ected by persistent elevation of circulating adhesion molecules may be useful in predicting the risk of GDM and subsequent risk of
type 2 diabetes in women with history of GDM. Nevertheless, further research is warranted to characterize the longitudinal changes of circulating endothelial cell adhesion molecules during pregnancy and to compare the levels of these molecules between GDM pregnancy and normoglycemic pregnancy.
