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Metabolism ; 44(10): 1308-13, 1995 Oct.
Article in English | MEDLINE | ID: mdl-7476290

ABSTRACT

We have shown that preeclampsia is associated with insulin resistance. In the present study, we examined young normal, preeclamptic (PE), and gestational hypertensive (GH) nulliparous African-American women at term to investigate cellular determinants of this resistance and insulin and insulin-like growth factor-I (IGF-I) binding to partially purified erythrocyte receptors and receptor tyrosine kinase activity (TKA). Blood pressure was significantly elevated in PE and GH subjects as compared with controls. Insulin binding was similar in number and affinity in the three groups (femtomoles per microgram). IGF-I binding was increased in PE subjects as compared with either normals or GH subjects (0.2 +/- 0.02, 0.15 +/- 0.01, and 0.14 +/- 0.02 fmol/microgram protein). Insulin receptor TKA was increased in PE subjects as compared with normals when assessed either per microgram protein or per femtomole insulin binding (P < .01). In contrast, IGF-I-potentiated TKA was elevated in PE subjects only when assessed per microgram protein (P < .03). Thus, the increased number of IGF-I receptors in erythrocytes of PE subjects yields a net increase in receptor tyrosine kinase. Also, there is an augmentation of insulin receptor TKA in PE subjects. Together, these two alterations may be a compensatory mechanism for the insulin resistance associated with hypertensive diseases of pregnancy.


Subject(s)
Erythrocytes/chemistry , Hypertension/blood , Insulin/blood , Pregnancy Complications, Cardiovascular/blood , Protein-Tyrosine Kinases/blood , Receptor, IGF Type 1/analysis , Adult , Black People , Blood Pressure/physiology , Cell Separation , Erythrocytes/cytology , Female , Humans , Hypertension/enzymology , Hypertension/physiopathology , Insulin/metabolism , Insulin Resistance/physiology , Pregnancy , Pregnancy Complications, Cardiovascular/enzymology , Pregnancy Complications, Cardiovascular/physiopathology , Protein-Tyrosine Kinases/metabolism , Receptor, IGF Type 1/metabolism
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