Insulin-dependent Diabetic Women Research Articles

Oral Administration of Magnesium Hydroxide to Subjects with Insulin-dependent Diabetes Mellitus: Effects on Magnesium and Potassium Levels and on Insulin Requirements

Introduction: Diabetics lack potassium and magnesium. (Mg). Hypokalemia and hypomagnesemia cause vasoconstriction and glucose breakdown, so all hypomagnesemia diabetics should take K and Mg daily to prevent diabetic arterial disease. Methodology: 80 types 1 diabetes (T1-DM) patients were analyzed for parameters like K, Mg, Serum, Lipids, and HBA1c. After giving 1.7mg/dL blood Mg patients, 300mg Mg oxide daily for 3 months, the parameters were re-examined. 40 insulin-dependent diabetic men and women averaged 16.79 ± 4.00 years, Mg 2.94.38/dL. 30.3% had hypomagnesemia. Blood magnesium levels are inversely associated with age, diabetes length (P value 0.002) and other parameters and are favourably correlated with mean corpuscular volume, HDL, and platelet counts. Mg supplementation substantially lowered HBA1c. HBA1c started at 09.22%1.98%. Oral K and Mg tablets for three months lower it to 6.77%1.53%. (P0.003). it also lowered LDL, blood lipids, and total cholesterol in hypomagnesemia diabetics. Conclusion: Oral Mg intake in T1-DM patients improves glucose control, atherogenic lipid proportion, and therapeutic lipid component.

Antepartum pudendal neuropathy and the effect of vaginal delivery in women with type 1 diabetes mellitus in pregnancy

Vaginal delivery is associated with a significant risk of pelvic floor neuropathy and anal sphincter dysfunction. Becauseinsulin-dependent diabetes mellitus (IDDM) predisposes to neuropathy, our aim was to determine the incidence of pudendalnerve dysfunction in a cohort of pregnant insulin-dependent diabetic patients and to examine the effect of vaginal delivery onpudendal nerve and anal sphincter function. Materials and Methods: The pudendal nerve was evaluated usingelectromyography of the anal sphincter (EMG) and clitoral anal reflex (CAR) assessment, during the third trimester in 16pregnant insulin-dependent diabetic women. Upper limb neurological assessment included median motor, ulnar f-wave,median and ulnar sensory nerve and median transpalmar nerve conduction studies, while the lower limbs were assessed usingtibial motor and f-wave studies. Anal manometry and endoanal ultrasound studies were also performed. Thirteen womenunderwent full reassessment at three months postpartum. Results: An increased sensory threshold (>9mA) on CAR wasdemonstrable antenatally in 5 women on the right and 8 on the left. Seven women showed prolonged distal latency (>42ms)on the right and in 8 on the left. Five women showed prolongation of median transpalmar nerve conduction studies (>2.2ms),which was associated with diabetes of greater than 12 years duration (p=0.029). The median squeeze pressure was 129mmHgand median resting pressure was 62mmHg. There were no significant changes in nerve conduction or anal manometricpressures postnatally. Discussion: Pregnant women with type 1 IDDM exhibit subtle changes of axonal neuropathy anddemyelination, but we found no increased susceptibility to pudendal nerve injury during vaginal childbirth. (Int J DiabetesMetab 14: 82-86, 2006 )

Impact of pre-gestational and gestational diabetes mellitus on the expression of glucose transporters GLUT-1, GLUT-4 and GLUT-9 in human term placenta

PurposeVarious studies in placental tissue suggest that diabetes mellitus alters the expression of glucose transporter (GLUT) proteins, with insulin therapy being a possible modulatory factor. The aim of the present study was quantitative evaluation of the expression of glucose transporters (GLUT-1, GLUT-4, GLUT-9) in the placenta of women in both, uncomplicated and diabetic pregnancy. Additionally, the effect of insulin therapy on the expression of selected glucose transporter isoforms was analyzed.MethodsTerm placental samples were obtained from healthy control (n = 25) and diabetic pregnancies, including diet-controlled gestational diabetes mellitus (GDMG1) (n = 16), insulin-controlled gestational diabetes mellitus (GDMG2) (n = 6), and pre-gestational diabetes mellitus (PGDM) (n = 6). Computer-assisted quantitative morphometry of stained placental sections was performed to determine the expression of selected glucose transporter proteins.ResultsMorphometric analysis revealed a significant increase in the expression of GLUT-4 and GLUT-9 in insulin-dependent diabetic women (GDMG2 + PGDM) as compared to both, control and GDMG1 groups (p < .05). Significantly increased GLUT-1 expression was observed only in placental specimens from patients with PGDM (p < .05). No statistically significant differences in GLUT expression were found between GDMG1 patients and healthy controls.ConclusionsThe results of the study confirmed the presence of GLUT-1, GLUT-4 and GLUT-9 proteins in the trophoblast from both, uncomplicated and diabetic pregnancies. In addition, insulin therapy may increase placental expression of GLUT-4 and GLUT-9, and partially GLUT-1, in women with GDMG2/PGDM.

Erythrocyte Na +–Li + counter-transport activity and digoxin-like substances in insulin dependent diabetic women with preexisting preeclampsia

Aim of the study To determine whether there is pathogenetic link between red cells sodium–lithium counter-transport activity and digoxin-like immunoreactive substances (DLIS) in plasma of insulin-dependent diabetic (IDDM) and non-diabetic women with preexisting preeclampsia (PE). Subjects and methods We studied Na +/Li + CT activity in red cells and plasma levels of DLIS in 11 IDDM women with preexisting PE (Group 1), 13 IDDM without preexisting PE (Group 2) 23 non-diabetic women with preexisting PE (Group 3) and 12 non-diabetic women with normal pregnancy (Group 4) at least 4 months after delivery. Results Na +/Li + CT activity was higher in Group 1 compared to Group 2 (mean ± SEM 0.316 ± 0.05 vs 0.190 ± 0.02 mmol/LRBC/hr p < 0.05) and in Group 3 compared to Group 4 (0.365 ± 0.004 vs 0.168 ± 0.01 mmol/LRBC/hr, p < 0.01). Plasma levels of DLIS were higher in Group 3 compared to Group 4 (0.727 ± 0.189 vs 0.295 ± 0.066 ng/ml; p < 0.05); there was no statistically significant difference between the two diabetic groups. In Groups 1 and 3, Na +/Li + CT activity was correlated to the plasma levels of DLIS ( r = 0.927; p < 0.001 and r = 0.485; p < 0.05 respectively). Conclusion Increased Na +/Li + CT activity and increased plasma levels of DLIS may contribute to PE in IDDM and non-diabetic women.

Fetal growth trajectories in Type‐1 diabetic pregnancy

To describe the individual intrauterine growth patterns of fetuses of insulin-dependent (Type-1) diabetic women and to examine determinants of overgrowth (macrosomia) and its timing. This retrospective longitudinal study examined the developmental trajectories of fetal abdominal circumference (AC) and biparietal diameter in 76 Type-1 diabetic women with singleton pregnancies. Latent class analysis was used to identify subgroups of patients with a shared fetal AC growth trajectory. Subsequently, maternal factors, including glycemic control as assessed by glycosylated hemoglobin (HbA1c), were examined to see whether they had any effect on fetal growth. Four subgroups with different AC growth patterns were identified. Differences in birth weight between the distinct subgroups were related to the shape of the AC growth velocity curve over gestation. Acceleration of AC growth commencing before or after 25 weeks' gestation was associated with the birth of a heavy or large-for-dates baby in 94 and 56% of cases, respectively. Poor glycemic control (HbA1c > 7.0%) during the periconception period or before 12 weeks' gestation was a modest predictor of midtrimester growth in AC. Other diabetes-related factors, fetal sex, parity, or maternal weight/obesity were unrelated to the fetal growth pattern. The findings suggest that an individual fetus's growth trajectory is set early in gestation and that the contemporaneous degree of maternal glycemia plays a role in determining birth weight.

Diagnostic value of continuous wave (cw) Doppler sonography in maternal diabetes mellitus

Doppler studies of umbilical, uterine and arcuate artery velocity wave forms were performed in 40 insulin-dependent diabetic women in the first and second half of pregnancy. Using a continuous-wave Doppler device, the resistance index (RI) was calculated to determine the degree of vascular resistance in utero-placental and foeto-placental compartment. The 90th percentile was used to classify flow velocity profiles. In addition, diastolic notching and incomplete registration of uterine and arcuate arteries were considered as an abnormal result in utero-placental perfusion. The prevalence of abnormal velocity wave forms in this risk group was higher than in a non-diabetic population. No significant correlation was found between abnormal Doppler studies and White's classification. Patients with vasculopathy represent a high-risk group for foetal growth retardation, which may be detected early by umbilical and especially uterine artery Doppler studies. Abnormal uterine and arcuate artery wave forms allowed identification of patients who developed pregnancy-induced hypertension/preeclampsia.

The influence of tobacco smoking on humoral immune response in insulin dependent diabetic pregnancy

Tobacco smoking products have a heavy impact on the public health of developed as well as non-developed countries by being a main etiologic factor for the induction of cardiovascular diseases and tobacco-related cancer. The purpose of this study was to determine the influence of tobacco smoking on the measurement of the humoral immune response in Egyptian pregnant women with type 1 diabetes. Concentrations of serum immunoglobulin A, G and M in 35 smoking, 35 non-smoking pregnant women with type 1 diabetes and 35 matched normal women were measured by ELISA. Women were matched by age and working life with controls. Measurements suggested that diabetic smokers had decreased levels of IgG and IgM in their sera. It was found that normal individuals had mean IgA, IgG and IgM levels of 2.80 mg/ml, 9.33 mg/ml and 1.66 mg/ml, respectively while non-smoker women suffering from type 1 diabetes had mean levels of 3.47 mg/ml, 10.97 mg/ml and 2.05 mg/ml (p<0.0004,p<0.0001 andp<0.0002). However, the mean level of IgA, IgG and IgM in diabetic smoker sera was determined to be 3.33 mg/ml, 8.07 mg/ml and 1.31 mg/ml, respectively (p<0.003,p<0.0001 andp<0.0001). The obtained results suggest that toxic smoke components were immuno-suppressant and may well play a part in the complex immuno-pathogenesis interaction. The increased risk of smoking in insulin dependent diabetic pregnant women during pregnancy is a further reason to encourage pregnant women to quit tobacco smoking.

Glycosylated Hemoglobin and Protein Levels in Normal and Diabetic Pregnancies

DOI: http://dx.doi.org/10.5915/17-2_3-12756 The glycosylated fractions of hemoglobin i.e. Glycohemoglobin (GlycoHb) and of the plasma proteins i.e. Glycoprotein (GlycoPR) levels were quantitated using an affinity chromatographic technique in the cord and maternal blood of normal (Group I), White's Class A diabetic (Group II), and insulin-dependent diabetic (Group III) women. There was a significant increase of GlycoHb and GlycoPR levels in Group III compared lo Group I neonates. Maternal GlycoHb but not GlycoPR levels were significantly higher in Group Ill patients. Maternal and cord blood GlycoHb and GlycoPR levels in Class A diabetics were not different from those levels in the normal group. We conclude that the fetuses of insulin-dependent diabetic mothers are hyperglycemic in utero.

Insulin dose during glucocorticoid treatment for fetal lung maturation in diabetic pregnancy: test of an algorithm [correction of analgoritm

Poor glycemic control is often a serious clinical problem during glucocorticoid treatment for fetal lung maturation in pregnant women with diabetes. An algorithm for improved subcutaneous insulin treatment during glucocorticoid treatment in insulin-dependent diabetic women was developed and tested. The sample, divided into two cohorts, consisted of all insulin-dependent diabetic women (n=16) receiving glucocorticoid treatment (betamethasone 12 mg i.m., repeated after 24 h) from 1996 to 1999. In the first cohort the increments of insulin dose were based on the level of blood glucose obtained. Based on the first cohort an algorithm to determine increments of insulin dose was developed. In the second cohort (n = 8) the insulin dose was increased by up to 40%, according to the algorithm, starting immediately after glucocorticoid treatment; prior to a detectable increase in blood glucose. After betamethasone, the daily insulin dose for the following 5 days was increased by 6, 38, 36, 27 and 17% in the first cohort vs. 27, 45, 40, 31 and 11% in the second cohort. The algorithm was used in the second cohort. The median blood glucose was 6.7, 14.3, 12.3, 7.7 and 7.7 vs. 7.7, 8.2, 9.6, 7.0 and 7.4 mmol/l (p<0.05 for day 2 and 3) in the two cohorts, respectively. None developed ketoacidosis or severe hypoglycemia. An algorithm with an increasing insulin dose of up to 40% shortly after glucocorticoid treatment for fetal lung maturation in diabetic women prevents severe dysregulation of metabolic control.

This month in J Lab Clin Med: Issue highlights for December 2000

This month in J Lab Clin Med: Issue highlights for December 2000

Outcome of Diabetic Pregnancy With Spontaneous Labour After 38 Weeks

Previously, the risk of intrauterine death in term infants of diabetic mothers led to elective delivery at 38 weeks, after confirmation that the lungs were mature. This study looked at perinatal outcomes in 148 women with well-controlled insulin-dependent diabetes who were allowed to enter labor spontaneously. All of them had reached 38 weeks with a live fetus, no obstetrical complications, and fasting blood glucose levels of 3 to 5 mM/liter (with 2-hour postprandial levels <7 mM/liter) through most of the pregnancy. One-third of the group were primigravidas. Half of the women delivered between 38 and 39 weeks’ gestation, and the rest delivered at 40 to 42 weeks’ gestation. Instrumental delivery was performed in 9 percent of cases, and cesarean delivery was performed in 7 percent. The two perinatal deaths yielded a perinatal mortality rate of 13.5 per 1000. Twenty-one infants, 14 percent of those born, required admission to a special care unit. The major differences from the general hospital population were a higher rate of operative delivery in labor (7 vs. 3.4 percent) and a higher proportion of newborn infants weighing 4 kg or more (33 vs. 18 percent). Nevertheless, there was only one case of shoulder dystocia in the diabetic group. In a larger group of 373 insulin-dependent diabetic women, from whom the study population was selected, the perinatal mortality was 3-fold greater than in the general hospital population (32 vs. 10.6 per 1000). In the well-controlled diabetic patients, the last glycosylated hemoglobin level before delivery did not predict either high birth weight or the need for cesarean delivery. Vaginal delivery is the norm in well-controlled women with insulin-dependent diabetes who are allowed to enter labor spontaneously after 38 weeks’ gestation. Perinatal morbidity and mortality are not excessive, and the risk of shoulder dystocia is not increased. Ir J Med Sci 1999;168:160–163

Inositol Phosphoglycans and Signal Transduction Systems in Pregnancy in Preeclampsia and Diabetes: Evidence for a Significant Regulatory Role in Preeclampsia at Placental and Systemic Levels

Measurements have been made of the urinary content of inositol phosphoglycans IPG P-type and IPG A-type, putative insulin second messengers, in preeclampsia, in type I insulin-treated diabetic pregnant women and their matched control subjects, and nonpregnant women of child-bearing age. The content of IPG P-type and IPG A-type was also measured in the placenta from preeclamptic patients and from normal pregnancies. Pregnancy was associated with an increase, approximately twofold, in urinary output of IPG-P-type relative to nonpregnant controls (P < 0.01). The 24-h output of IPG P-type in urine in preeclamptic women was significantly higher (2- to 3-fold) than in pregnant control subjects matched for age, parity, and stage of gestation (P < 0.02). In contrast, insulin-dependent diabetic pregnant women did not show any significant change in urinary output of IPG P-type or IPG A-type relative to pregnant control subjects. Evidence for a possible relationship and correlation between the urinary excretion of IPG P-type and markers of preeclampsia, including proteinuria (r = 0.720, P < 0.01), plasma aspartate transaminase (r = 0.658, P < 0.05), and platelet counts (r = 0.613, P < 0.05) is presented. A high yield of IPG P-type was extracted from human placenta, in preeclampsia some 3-fold higher (P = 0.03) than the normal value, whereas no IPG A-type (with lipogenic-stimulating activity) was found. Low concentrations of placental IPG A-type were detected relative to IPG P-type using assay systems dependent upon the effect of this mediator on cAMP-dependent protein kinase or on a proliferation assay using thymidine incorporation into DNA of EGFR T17 fibroblasts. It is postulated that the high urinary excretion IPG P-type in preeclampsia reflects high placental levels and relates to the accumulation of glycogen in the placenta. The paracrine effects of placental IPG P-type (stimulation off other endocrine glands and/or endothelial cells) could contribute to the pathogenesis of the maternal syndrome. A possible theoretical link between elevated placental IPG P-type and apoptosis is proposed.

Glycemic Control Throughout Pregnancy and Fetal Growth in Insulin-Dependent Diabetes

In Brief Objective To determine the time of growth acceleration in fetuses of insulin-dependent diabetic women who are large for gestational age (LGA) at birth and the relationship between growth acceleration and diabetic control throughout pregnancy. Methods We studied a consecutive sample of 76 women with insulin-dependent diabetes divided by those who delivered LGA or normally grown infants. Fetal abdominal circumference (AC) was measured ultrasonically at regular intervals between 20 and 34 weeks' gestation. Diabetic control was assessed by regular measurement of glycosylated hemoglobin and capillary blood glucose levels. Results A significant difference in fetal AC between groups developed between 20 and 24 weeks' gestation, and the LGA group continued to have accelerated fetal growth. Between 18 and 24 weeks glycosylated hemoglobin and capillary blood glucose concentrations were significantly higher in women who delivered LGA infants. After 28 weeks, blood glucose concentrations and glycosylated hemoglobin did not differ significantly between groups. There was a nonsignificant trend toward more vaginal deliveries in the normal group (45% versus 32%). Conclusion In insulin-dependent diabetic pregnancy, although actual growth acceleration occurred from about 20 weeks' gestation, growth potential of fetuses appeared to be determined by prevailing maternal glucose concentrations before then. Excessive growth continued despite subsequent satisfactory glucose control. If strict blood glucose control is maintained during first and second trimesters, it might reduce the incidence of LGA infants. Poor glycemic control during the second trimester in women with insulin-dependent diabetes was associated with subsequent fetal growth acceleration.

Glycemic control throughout pregnancy and fetal growth in insulin-dependent diabetes

Objective: To determine the time of growth acceleration in fetuses of insulin-dependent diabetic women who are large for gestational age (LGA) at birth and the relationship between growth acceleration and diabetic control throughout pregnancy. Methods: We studied a consecutive sample of 76 women with insulin-dependent diabetes divided by those who delivered LGA or normally grown infants. Fetal abdominal circumference (AC) was measured ultrasonically at regular intervals between 20 and 34 weeks’ gestation. Diabetic control was assessed by regular measurement of glycosylated hemoglobin and capillary blood glucose levels. Results: A significant difference in fetal AC between groups developed between 20 and 24 weeks’ gestation, and the LGA group continued to have accelerated fetal growth. Between 18 and 24 weeks glycosylated hemoglobin and capillary blood glucose concentrations were significantly higher in women who delivered LGA infants. After 28 weeks, blood glucose concentrations and glycosylated hemoglobin did not differ significantly between groups. There was a nonsignificant trend toward more vaginal deliveries in the normal group (45% versus 32%). Conclusion: In insulin-dependent diabetic pregnancy, although actual growth acceleration occurred from about 20 weeks’ gestation, growth potential of fetuses appeared to be determined by prevailing maternal glucose concentrations before then. Excessive growth continued despite subsequent satisfactory glucose control. If strict blood glucose control is maintained during first and second trimesters, it might reduce the incidence of LGA infants.

The effect of maternal exercise on umbilical artery blood flow in insulin-dependent diabetics

Nine insulin-dependent diabetic women underwent a moderate exercise test. The mean exercise intensity achieved was 65% (50-80%) of submaximal exercise. The maternal heart rate rose significantly after exercise from a mean of 85 b.p.m. (60-109 b.p.m.) to a mean of 140 b.p.m. (112-168 b.p.m.). Maternal systolic blood pressure rose significantly from a mean of 115 mmHg (90-130 mmHg) to a mean of 157 mmHg (145-180 mmHg). The diastolic blood pressure also rose, but insignificantly, from a mean of 71 mmHg (65-90) mmHg to a mean of 85 mmHg (80-90) mmHg after exercise. The mean umbilical pulsatility index (PI) showed significant decrease at 2 and 6 minutes of recovery from exercise and subsequently showed a significant rise after 20 minutes. This rise continued even after a full 30 minutes of recovery from exercise.

A study on human umbilical cord endothelial cells: Functional modifications induced by plasma from insulin-dependent diabetes mellitus patients

The aim of the present study was to evaluate the action of plasma from insulin-dependent diabetic (IDDM) pregnant women on nitric oxide synthase (NOS) activity in cultured human umbilical vein endothelial cells (HUVECs). We also studied the effect of the plasma on cytosolic calcium and on Na + K + -adenosine triphosphatase (ATPase) activity. Dynamic fluorescence studies of membrane fluidity were contemporarily performed to detect a direct effect of plasma on the endothelial cell membrane. We observed a significant increase in NOS activity, intracellular calcium, and Na + K + -ATPase activity in cultured HUVECs exposed to IDDM plasma. Our dynamic fluorescence study showed a different microenvironmental organization of the cellular membrane after incubation with plasma from IDDM pregnant women, with a marked decrease in microheterogeneity as evaluated in terms of 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH) lifetime distribution width. The present investigation suggests that plasma from IDDM pregnant women can cause a generalized disturbance in the function of endothelial cells cultured from healthy subjects. Such a modification might play a central role in the pathogenesis of the vascular complications of the disease.

Pregnancies Complicated by Diabetic Proliferative Retinopathy

Background. To examine retinal and pregnancy outcome in insulin-dependent diabetic women with proliferative retinopathy and assess the effect of albuminuria on morbidity. Methods. The records of 26 women with known proliferative retinopathy before pregnancy were studied retrospectively in the prepregnancy period, during pregnancy, and after delivery. Perinatal and maternal morbidity was studied using ophthalmic, obstetric and pediatric records. Results. Seven pregnancies were delivered preterm (27%). Serious neonatal morbidity occurred in five pregnancies (19%). Perinatal survival was 88%. Laser treatment was given prior to pregnancy to 54%, during pregnancy to 27% and after delivery to 31% of the women. Laser treatment during pregnancy was more common in those with no prior photocoagulation and in White class F/R. Low birthweight was more frequently associated with nephropathy and proliferative retinopathy compared to retinopathy alone (p<0.05). Recent hemorrhage, maculopathy or glaucoma was found in 14 (54%) of the women. Blindness developed unilaterally in two women. Conclusions. Perinatal morbidity was associated with nephropathy rather than retinopathy. The incidence of hemorrhage, maculopathy or glaucoma was similar in White classes R and F/R.

Pregnancies complicated by diabetic proliferative retinopathy

To examine retinal and pregnancy outcome in insulin-dependent diabetic women with proliferative retinopathy and assess the effect of albuminuria on morbidity. The records of 26 women with known proliferative retinopathy before pregnancy were studied retrospectively in the prepregnancy period, during pregnancy, and after delivery. Perinatal and maternal morbidity was studied using ophthalmic, obstetric and pediatric records. Seven pregnancies were delivered preterm (27%). Serious neonatal morbidity occurred in five pregnancies (19%). Perinatal survival was 88%. Laser treatment was given prior to pregnancy to 54%, during pregnancy to 27% and after delivery to 31% of the women. Laser treatment during pregnancy was more common in those with no prior photocoagulation and in White class F/R. Low birthweight was more frequently associated with nephropathy and proliferative retinopathy compared to retinopathy alone (p<0.05). Recent hemorrhage, maculopathy or glaucoma was found in 14 (54%) of the women. Blindness developed unilaterally in two women. Perinatal morbidity was associated with nephropathy rather than retinopathy. The incidence of hemorrhage, maculopathy or glaucoma was similar in White classes R and F/R.

Modifications induced by plasma from insulin-dependent diabetic patients and by lysophosphatidylcholine on human Na+,K(+)-adenosine triphosphatase.

To investigate the molecular mechanisms of the inhibition of Na+,K(+)-adenosine triphosphatase (Na+,K(+)-ATPase) in diabetes mellitus, we incubated Na+,K(+)-ATPase purified from human placenta of six healthy nondiabetic women with plasma from six insulin-dependent diabetic (IDDM) men and six healthy controls and with different concentrations of lysophosphatidylcholine (LPC). We determined the enzyme activity, anthroyl ouabain-binding capacity, dissociation constant (Kd), and average lifetime values (tau) by the static and dynamic fluorescence of anthroyl ouabain. The lipid annulus of the enzyme was studied by static and dynamic fluorescence of 1-(4-trimethylamino-phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). Moreover, we studied the lipid microenvironment surrounding the Na+,K(+)-ATPase purified from the placentas of six healthy women and six insulin-dependent diabetic women, determining the percent composition of phospholipids of the lipid annulus. The addition of total and protein-free IDDM plasma to normal Na+,K(+)-ATPase significantly inhibited the enzymatic activity even at the lowest concentration studied (1: 100), whereas the ouabain-binding capacity, Kd, and tau were not affected by IDDM plasma. The fluorescence polarization and lifetime values of TMA-DPH were significantly decreased by diabetic plasma. The incubation of Na+,K(+)-ATPase with LPC caused an inhibition of the enzymatic activity without modifications of the anthroyl ouabain-binding capacity and dissociation constant. The fluorescence polarization and lifetime values of TMA-DPH were significantly decreased by 5 mumol/L LPC. The study of the phospholipids surrounding Na+,K(+)-ATPase demonstrated a significant increase in the percent LPC content in IDDM patients compared with controls together with a concomitant decrease in phosphatidylcholine. These observations indicate that the inhibition caused by diabetic plasma on Na+,K(+)-ATPase is not dependent on a modification of the ouabain-binding site and that it seems to mimic the effect of LPC addition. A link between modification of the lipid moiety of the enzyme and Na+,K(+)-ATPase inhibition might be hypothesized.

Pregnancy Does Not Induce or Worsen Retinal and Peripheral Nerve Dysfunction in Insulin-Dependent Diabetic Women

In order to verify whether pregnancy induces or worsens diabetic retinopathy or somatic and autonomic neuropathy, 16 insulin-dependent diabetic (IDDM) pregnant women, 14 age-matched nondiabetic pregnant women, and 12 IDDM nonpregnant women matched for age and disease duration were studied. Plasma glucose, HbA 1c, and fructosamine were repeatedly assayed during pregnancy. Retinopathic and neuropathic endpoints were evaluated through ophthalmoscopy, electrophysiology of left peroneal and sural nerves (motor and sensory conduction velocities), and cardiovascular autonomic tests (deep breathing, cough test, lying-to-standing). In the IDDM pregnant women, evaluations were performed three times during pregnancy and 6 months after delivery. Good metabolic control was achieved during pregnancy. At baseline, nine IDDM pregnant women did not show signs of retinopathy, and seven had nonproliferative retinopathy. Only one patient showed worsening during pregnancy, but she improved after delivery. Motor conduction velocity, significantly lower in IDDM pregnant women, progressively improved, and, in the third trimester, was not significantly different from that of nondiabetic pregnant women. At baseline, none of the IDDM pregnant women had abnormal responses to cardiovascular autonomic tests. During pregnancy, the response to deep breathing appeared temporarily reduced in all pregnant women, possibly due to lowered ventilatory excursion at the end of pregnancy. In IDDM women with minimal or no retinopathy, and subclinical or no peripheral neuropathy, pregnancy does not appear to induce or worsen these complications.