کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3961734 | 1255619 | 2009 | 6 صفحه PDF | دانلود رایگان |

In preeclampsia, there is exacerbation of physiological changes associated with pregnancy such as insulin resistance, altered immune responses and inflammatory pathway activation. These exaggerated responses seen in preeclampsia are reminiscent of metabolic syndrome, and also are evident in gestational diabetes mellitus. The link between these phenomena is not clear but novel findings providing some insight have been reported recently. Inositol phosphoglycan P-type (P-IPG) in preeclampsia has been extensively investigated and increased production has been demonstrated. This molecule acts as a second messenger of insulin, enhances the metabolic effects of insulin and is associated with insulin resistance. This review article summarizes current evidence of the role of inositol phosphoglycans in the metabolic syndrome that occurs in preeclampsia, discussed in the light of modifications found in gestational diabetes mellitus and diabetes type 2 in pregnancy in humans and animal models. An increase in urinary release of P-IPG during pregnancy may herald the onset of preeclampsia. Further knowledge about the nature of the metabolic syndrome during preeclampsia and the degree of association between its components will help to inform future research efforts and to identify biochemical markers that could help in clinical practice, for example early markers that will have utility in managing disease progression.
Journal: Journal of Reproductive Immunology - Volume 82, Issue 2, November 2009, Pages 100–105