Na(+)/K(+)-ATPase activity and expression in syncytiotrophoblast plasma membranes in pregnancies complicated by diabetes.

Many of the transport processes across the syncytiotrophoblast (ST), such as amino acid transport, are Na(+)-coupled. The maintenance of a low intracellular Na(+) concentration by Na(+)/K(+)-ATPase is therefore crucial for placental transport of nutrients and consequently, foetal growth. In pregnancies complicated by diabetes foetal growth is often accelerated despite rigorous glycemic control of the mother, however the underlying mechanisms are not fully understood. We tested the hypothesis that Na(+)/K(+)-ATPase in ST plasma membranes is up-regulated in diabetic pregnancies associated with accelerated growth. ST microvillous (MVM) and basal (BM) plasma membranes were purified from term placentas of normal pregnancies (control, n=13) and pregnancies complicated by insulin-dependent diabetes mellitus (n=7) or gestational diabetes (n=6). All mothers with diabetes gave birth to large for gestational age babies. The Na(+)/K(+)-ATPase alpha(1)-subunit protein expression (Western blot) in MVM and BM was unaltered by diabetes. Na(+)/K(+)-ATPase activity (K(+)-stimulated, ouabain-sensitive phosphatase activity) in ST plasma membranes was not affected by diabetes. This is the first study of Na(+)/K(+)-ATPase in ST membranes of the human placenta in diabetes. Our data show that accelerated foetal growth in diabetic pregnancies is not associated with elevated ST Na(+)/K(+)-ATPase protein expression or activity.

[1]  P. Palatini,et al.  Reduction of erythrocyte (Na+-K+)ATPase activity in Type 1 (insulin-dependent) diabetic subjects and its activation by homologous plasma , 1986, Diabetologia.

[2]  T. Powell,et al.  Na(+)-K(+)-ATPase is distributed to microvillous and basal membrane of the syncytiotrophoblast in human placenta. , 2000, American journal of physiology. Regulatory, integrative and comparative physiology.

[3]  N. Illsley,et al.  Diabetes alters the expression and activity of the human placental GLUT1 glucose transporter. , 1999, The Journal of clinical endocrinology and metabolism.

[4]  T. Powell,et al.  Placental glucose transport and GLUT 1 expression in insulin-dependent diabetes. , 1999, American journal of obstetrics and gynecology.

[5]  D. Raccah,et al.  Erythrocyte Na/K ATPase activity and diabetes: relationship with C-peptide level , 1998, Diabetologia.

[6]  E. Amler,et al.  Modifications induced by plasma from insulin-dependent diabetic patients and by lysophosphatidylcholine on human Na+,K(+)-adenosine triphosphatase. , 1998, The Journal of clinical endocrinology and metabolism.

[7]  P. Kvasnička,et al.  Modifications induced by insulin-dependent diabetes mellitus on human placental Na+/K+-adenosine triphosphatase. , 1997, The Journal of laboratory and clinical medicine.

[8]  A. Selbing,et al.  Intrauterine growth curves based on ultrasonically estimated foetal weights , 1996, Acta paediatrica.

[9]  P. Garner Type I diabetes mellitus and pregnancy , 1995, The Lancet.

[10]  P. Bennett,et al.  Diabetes and Obesity in the Offspring of Pima Indian Women With Diabetes During Pregnancy , 1993, Diabetes Care.

[11]  H. Adami,et al.  Evidence of prenatal influences on breast cancer risk , 1992, The Lancet.

[12]  J. Pouget,et al.  Hypothesis: low Na/K-ATPase activity in the red cell membrane, a potential marker of the predisposition to diabetic neuropathy. , 1992, Diabete & metabolisme.

[13]  P. Bennett,et al.  Abnormal Glucose Tolerance During Pregnancy in Pima Indian Women: Long-Term Effects on Offspring , 1991, Diabetes.

[14]  N. Illsley,et al.  Simultaneous preparation of paired, syncytial, microvillous and basal membranes from human placenta. , 1990, Biochimica et biophysica acta.

[15]  D. Greene,et al.  Sorbitol, phosphoinositides, and sodium-potassium-ATPase in the pathogenesis of diabetic complications. , 1987, The New England journal of medicine.

[16]  D. Greene,et al.  Decreased Myo-Inositol Content and Na+-K+-ATPase Activity in Superior Cervical Ganglion of STZ-Diabetic Rat and Prevention by Aldose Reductase Inhibition , 1986, Diabetes.

[17]  F. Matschinsky,et al.  Altered retinal metabolism in diabetes. II. Measurement of sodium-potassium ATPase and total sodium and potassium in individual retinal layers. , 1986, The Journal of biological chemistry.

[18]  E. F. Kern,et al.  Basal phosphatidylinositol turnover controls aortic Na+/K+ ATPase activity. , 1986, The Journal of clinical investigation.

[19]  A. Dasmahapatra,et al.  Reduced Glomerular Sodium/Potassium Adenosine Triphosphatase Activity in Acute Streptozocin Diabetes and Its Prevention by Oral Sorbinil , 1985, Diabetes.

[20]  P Q Peterson,et al.  Macrosomia—Maternal Characteristics and Infant Complications , 1985, Obstetrics and gynecology.

[21]  D. Hill,et al.  FETAL GROWTH CONTROL: THE ROLE OF INSULIN AND RELATED PEPTIDES , 1984, Clinical endocrinology.

[22]  M. Waters,et al.  An automated fluorometric assay for alkaline phosphatase using 3-O-methylfluorescein phosphate. , 1968, Analytical biochemistry.

[23]  R. Mccomb,et al.  A continuous spectrophotometric method for measuring the activity of serum alkaline phosphatase. , 1966, Clinical chemistry.

[24]  J. Pedersen Weight and length at birth of infants of diabetic mothers. , 1954, Acta endocrinologica.

[25]  P. White Pregnancy complicating diabetes. , 1946, Pennsylvania medical journal.