Endocrine Abstracts (2007) 13 P264

Retinol binding protein 4 suppresses during normal pregnancy – an inverse relationship with insulin resistance

Michael Pierides1, Krzysztof Lewandowski2, Jeanette Bennet2, Diane Dunlop2, Harpal Randeva1 & Paul O’Hare1


1University Hospitals Coventry Warwickshire, Coventry, United Kingdom; 2University of Warwick – Warwick Medical School, Coventry, United Kingdom.


Retinol binding protein-4 (RBP4) is an adipokine reportedly linked to physiological states of insulin resistance and impaired glycaemia. Pregnancy is a physiological state characterised by changes in carbohydrate metabolism and increased insulin resistance. Our aim was to determine plasma levels of RBP4 during early pregnancy, late pregnancy and postpartum in normal women.

Fasting plasma levels of RBP4, insulin and glucose were collected and assayed (ELISA) in 12 pregnant women. They were followed at 20 weeks, 30 weeks and postpartum (non-lactating). Local Ethical Committee approval was obtained.

In normal pregnant women there was a highly significant lowering of RBP4 compared to the postpartum state. RBP4 levels (mmol/L) were lower at 20 weeks (mean 12.8,± S.D. 2.0) and at 30 weeks (12.6±2.8) compared to postpartum (19.4±5.7, P<0.001). There was no statistical difference between the second and third trimester. Fasting blood glucose (mmol/L) and insulin (mmol/L) levels taken at 0800 am had the following values: glucose at 20 weeks (3.8±0.5), 30 weeks (3.7±0.6) and postpartum (4.2±0.4). Conversely there was a significant change in insulin levels at 20 weeks (6.2±1.08), 30 weeks (7.2±1.6) and postpartum (4.4±1.06), P<0.02. This change is inversely related to the pattern shown by RBP4.

In conclusion, RBP4 levels showed a 33.7% drop during the physiological state of pregnancy compared to the non-pregnant postpartum state. Pregnancy is a physiological condition when RBP4 does not appear to reflect changes in insulin resistance. Most binding proteins derived from the liver increase in pregnancy. The suppression of RBP4 in pregnancy may be a physiological response to insulin resistance and impaired glycaemia in pregnancy. This could be an epiphenomenon or a primary phenomenum and may have implications in the physiology of retinoids and related proteins during pregnancy.

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