Expression of Adiponectin Receptors in Human Placenta and Its Possible Implication in Gestational Diabetes

Abstract

Problem statement: Similar to obese patients and type 2 diabetic patients, adiponectin levels are reduced in former Gestational Diabetes Mellitus (GDM) patients and are lower in GDM women during late pregnancy compared with pregnant control subjects matched for BMI. Diabetic insult at later stages in gestation, such as may occur in gestational diabetes, will foremost lead to shortterm changes in a variety of molecules for key functions including gene expression in the placenta. Approach: In this study we assessed the expression of adiponectin receptors in human placenta to identify the site (s) of expression and to clarify the effect of gestational diabetes in this expression. This study was carried on 10 normoglycemic pregnant women and 20 GDM women. The placental tissue was collected immediately after delivery and tissue biopsies were taken from both fetal and maternal sides of each placenta. One step-RT-PCR for ADIPOR1 and ADIPOR2 was done by Real Time PCR using Syber Green technique. Relative quantification of mRNA of the ADIPOR1 and ADIPOR2 genes was measured using ABI7900 Real Time machine. Results: Both types of Adiponectin Receptors (ADIPOR1 and ADIPOR2) are expressed in human placenta. ADIPOR1 is more highly expressed than ADIPOR2 in both fetal and maternal sides of GDM cases and normal pregnant women. ADIPOR1 mRNA expression was significantly up regulated in GDM women compared to normal pregnant women, whereas no significant difference in the expression of ADIPOR2 was detected between the two groups. There was no evidence of maternal-fetal side difference in the expression of adiponectin receptors in GDM cases but in normal pregnant women there is a statistically significant difference between both sides in the expression of both ADIPOR1 and ADIPOR2. Conclusion: We concluded that adiponectin plays an important role in mediation the glucose metabolism in fetal tissues through its receptors, mainly Adiponectin Receptor 1 (ADIPOR1).

Maternal obesity influences expression and DNA methylation of the adiponectin and leptin systems in human third-trimester placenta

“…Further experiments are in progress in our laboratory. Lastly, we showed that in human placenta, ADIPOR2 is 10- to 100-fold less expressed than ADIPOR1 , as generally described in other tissues and cell types [52, 53]. Interestingly, we observed that maternal obesity is associated with a significantly lower ADIPOR1 m RNA expression on the maternal side of the placenta and a significantly lower ADIPOR1 protein expression in the whole placental tissue.…”

A comparative study between the effect of 17-β estradiol and angiotensin converting enzyme inhibitor on osteoporosis in ovariectomized rats

“…Because the samples of control group and also samples of treated group are used as calibrators, the expression levels are set to 1. Because the relative quantities of the OPG&RANKL gene are normalized against the relative quantities of the endogenous control B-actin gene fold expression changes are calculated using the equation 2 -ΔΔct in the study of Alhusseini et al (2010).…”

The Role of Adiponectin during Pregnancy and Gestational Diabetes

“…However, more sensitive techniques have determined that the placenta does not produce endogenous adiponectin [ 119 , 170 , 171 ]. Adiponectin in the maternal circulation does not cross the placenta; however, adiponectin receptors (ADIPOR1 and ADIPOR2) are present in the placenta [ 163 , 165 , 172 ]. Placental signalling by adiponectin receptors impacts nutrient transport and fetal growth [ 34 , 173 ].…”