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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conflicting data exist concerning maternal serum concentrations of placental hormones during pregnancy in women with diabetes mellitus. To resolve some of these discrepancies, women participating in the NICHD-Diabetes in Early Pregnancy Study were studied. In this collaborative study, pregnancy was identified within 21 days of conception by serum hCG measurements. We prospectively collected 185 blood samples from 35 insulin-dependent diabetic women and 166 blood samples from 31 control women, all between 5 and 37 weeks gestation. Serum concentrations of hCG, pregnancy-specific beta-1-glycoprotein, placental lactogen, and hCG alpha were measured serially. The relationship between serum hormone, fasting blood glucose, 1-h postprandial blood glucose, and glycosylated hemoglobin concentrations was compared. Serum hCG alpha levels were significantly lower in the diabetic women than in control women at multiple time points during the first and second trimesters, while no consistent differences in the serum concentrations of hCG or pregnancy-specific beta-1-glycoprotein were found between pregnant diabetic and control women. Serum placental lactogen levels were significantly lower in diabetic women at 9-10 weeks and 20 weeks gestation. There were no correlations between fasting blood glucose, 1-h postprandial blood glucose, or glycosylated hemoglobin and any of the placental protein levels in the diabetic women. These data are consistent with a defect in synthesis and/or secretion of hCG alpha by the cytotrophoblast during the first two trimesters of pregnancy in insulin-requiring diabetic women.
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PMID:Comparison of serum placental protein hormone levels in diabetic and normal pregnancy. 278 18

Our previous studies have suggested that elevated lactogen, increased glucose-stimulated insulin secretion, and increased beta-cell coupling are associated. To determine whether this association occurs under conditions of physiologically increased lactogen, we have studied the extent of dye coupling in rat islets during the later stage of pregnancy. These animals have high plasma lactogen levels in the form of placental lactogen, increased plasma insulin, and decreased plasma glucose. The fluorescent tracer, Lucifer yellow CH, was microinjected into central cells of islets from both pregnant and virgin rats, and the extent of transfer was quantitated by determining the projected area of dye spread. Two area measurements were made for each injection, one around the entire discernible fluorescent region ("outer") and another around the distinct brighter region of cells surrounding the injected cell ("inner"). Pregnancy increased dye transfer, as determined by both measurements. The outer area of dye transfer was 9047 +/- 775 microns2 for the islets from pregnant rats and 4699 +/- 391 microns2 for the islets from virgin rats (P less than .001). Similarly, pregnancy increased the inner area of dye transfer, 1447 +/- 161 microns2 for the islets from pregnant rats and 795 +/- 80 microns2 for the islets from virgin rats (P less than .001). These results support the hypothesis that elevated lactogen, increased glucose-stimulated insulin secretion, and increased beta-cell dye coupling are associated under physiological conditions. The study indicates that enhanced beta-cell coupling is part of the structural and functional adaptation that the islets undergo during a subject's pregnancy and demonstrates that the extent of beta-cell coupling is regulated by a physiological condition.
Diabetes 1988 Jul
PMID:Increased dye coupling in pancreatic islets from rats in late-term pregnancy. 329 8

Sex hormones play an important role in the control of glucose metabolism and insulin. Decreased glucose tolerance observed at the end of pregnancy in most cases remains within normal limits. Pregnancy has an important effect on the islets of Langerhans and on the growth of beta cellules. At the end of pregnancy, assimilation of glucose and triglycerides by maternal tissues is slowed and transfer to the fetus is favored. Hyperinsulinism persists but insulin resistance at the level of maternal tissue becomes very strong and the number of receptors declines. This late pregnancy insulin resistance has not been satisfactorily explained. The declining number of receptors may be a mechanism, or the "antiinsulin" pregnancy hormones which includes estrogens and progesterone may play a major role. Although other mechanisms have been proposed to explain the antiinsulin effect, the role of sex hormones and especially of progesterone (and synthetic progestins used in contraception) appears crucial. The presence of estrogen and progesterone receptors in the beta cellules of the islets of Langerhans suggests a direct effect of these hormones on the cellules. Estrogens however work by other mechanisms than insulin secretion. Experimental evidence indicates that during pregnancy, progesterone increases insulin release while human placental lactogen stimulates hyperplasia of the islets. The progestins derived from progesterone used in contraception have a parallel action. A slight elevation of blood sugar and insulinemia have been observed in oral contraceptive (OC) users. Only 3-5% of OC users develop true hyperglycemia. The changes are usually transitory and disappear on termination of OC use except in the small number of women predisposed to diabetes. The decreased glucose tolerance of OC users differs from true diabetes. Combined OCs favor vascular accidents and myocardial infarct in insulin-dependent diabetics. The mechanisms involved include deteriorating control of diabetes; effects on the serum lipids, coagulation factors, and blood pressure; and direct effects of estrogen on the vascular wall. Venous but not arterial vascular accidents decline with lower estrogen doses. Progestins probably play a more significant role from estrogens in decreasing glucose tolerance. Pregnanes, progestins derived from progesterone, do not appear to affect glucose tolerance. Among testosterone derivatives, the entrances decrease glucose tolerance slightly and the gonanes more strongly, also causing hyperinsulinism. But the new triphasic OCs with low levonorgestrel doses cause no significant changes in glucose tolerance even in women with histories of gestational diabetes. Long-acting progestin implants, vaginal rings, and injectables appear thus far to have minimal or no effects on glucose tolerance.
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PMID:[Sex hormones and the metabolism of carbohydrates]. 333 54

The possible involvement of growth hormone (GH) and human placental lactogen (HPL) in the development of diabetic tissue damage during pregnancy was studied in 16 insulin-dependent diabetic patients (IDDM), 8 gestational diabetic patients (GD) and 14 normal pregnant women. GH and HPL were elevated in pregnancies complicated by diabetes but, in contrast to the rise of HPL, GH declined throughout pregnancy in all the groups studied. The concentrations of neither correlated with plasma glucose, insulin requirement or duration of diabetes. HPL was positively correlated with urinary albumin excretion (UAE) in all 3 groups, but with blood pressure only in the IDDM group. There was also a significant and positive correlation in all patients between HPL at the end of pregnancy and placental weight. No evidence of serious tissue damage was found in either diabetic group. The vibration sensory threshold was unaffected by pregnancy and was similar to that of normal women. However, in the IDDM group UAE increased significantly postpartum when compared with second trimester values; they also had higher UAE than the other 2 groups post-delivery. A small but significant rise in diastolic blood pressure (DBP) was found in the 3 groups studied between the second and third trimester and pre-delivery. The same trend in systolic blood pressure (SBP) was seen in the diabetic groups. The IDDM had higher systolic and diastolic blood pressures than the normal women at all stages of gestation.
Diabetes Res 1986 Mar
PMID:High levels of growth hormone and human placental lactogen in pregnancy complicated by diabetes. 351 44

We assessed the factors influencing the birth weight of infants born to 83 women with insulin-dependent diabetes mellitus (IDDM) over a 5-yr period. Maternal glycosylated hemoglobin (HbA1) concentrations at delivery correlated with the percentile birth-weight ratios (r = .43, P less than .001) and indicated that approximately 18% of variance in the birth weight could be ascribed to glycemic control in the third trimester. Fetal macrosomia occurred in 22 (27%) pregnancies. When 20 of these pregnancies were compared closely with 20 nonmacrosomic pregnancies in diabetic women, the mothers of macrosomic infants were found to be more obese, have a history of previous macrosomic birth, and have higher concentrations of serum human placental lactogen and urinary estriols in the third trimester. Macrosomic pregnancy was further distinguished by accelerated fetal growth (judged by serial ultrasonography) from the 32nd wk of gestation and by biochemical (but asymptomatic) hypoglycemia in the neonate. In our study, no serious neonatal morbidity could be attributed to macrosomic pregnancy. Good glycemic control was attained in both groups, and no significant differences between the groups in overall glycemic control throughout pregnancy were noted. Thus, despite good glycemic control, macrosomia remains comparatively common in modern pregnancy complicated by IDDM, and factors other than maternal hyperglycemia must contribute to its etiology.
Diabetes Care
PMID:Macrosomia in pregnancy complicated by insulin-dependent diabetes mellitus. 367 77

It has been hypothesized that plasma triglyceride fatty acids may traverse the placenta and contribute to infant adiposity particularly in GDM pregnancy. It has also been hypothesized that high-density lipoproteins (HDL) can both deliver cholesterol to and remove cholesterol from the placenta. To determine if these maternal parameters are related to fetal growth in normal pregnancy, we have examined relationships of lipoprotein lipids, apoproteins, hormones, fuels, clinical chemistries, and maternal weight at 36 wk gestation to infant birth weight, birth weight ratio (birth weight corrected for gestational age), birth length, and head circumference in a cohort of pregnant women attending a prepaid health plan, Group Health Cooperative of Puget Sound. Associations were examined using a multivariate regression analysis of several groups of related variables. Results show that the birth weight and/or birth weight ratio are weakly positively associated with maternal very-low-density lipoprotein (VLDL) triglyceride and statistically significantly positively associated with apoprotein A-I, placental lactogen, estradiol, bilirubin, and maternal prepregnancy weight and pregnancy weight gain. Glucose and insulin predict birth weight only in pairwise analysis. Significant negative predictors of birth weight or birth weight ratio include VLDL cholesterol, apoprotein A-II, SGOT, and creatinine. Significant positive predictors of birth length include apoproteins A-I, placental lactogen, and maternal weight. Apoprotein A-II negatively predicts birth length. Only maternal prepregnancy weight predicts head circumference.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Jun
PMID:Relationships of infant birth size to maternal lipoproteins, apoproteins, fuels, hormones, clinical chemistries, and body weight at 36 weeks gestation. 392 27

Overt diabetes and gestational diabetes (1-2.5% of all pregnancies) has been related to perinatal mortality, increased macrosomia and increased frequency of other pregnancy complications. Human placental lactogen (hPL), a hormone similar to growth hormone, is produced by the placenta and is a potent antagonist to insulin action. While hPL's presence in maternal circulation induces a sparing effect on nutrients including glucose, it exacerbates diabetes during pregnancy and may well relate to other clinical complications. To explore possible regulation of hPL in diabetic pregnancy and specifically to examine gestational diabetes, we have evaluated the levels of placental mRNA coding for hPL synthesis as well as other parameters from diabetic and normal term patients. By in vitro translation assays using nuclease-treated reticulocyte lysate, no substantial differences in translatable hPL-mRNA were observed when comparing normal term (3.5% of total synthesis), gestational diabetic (3.4%) and Type C diabetic (3.5%). However, translatable hPL-mRNA in Type R diabetes which was 2.7% of total synthesis was slightly reduced in comparison to normal term. To determine more directly hPL-mRNA levels in gestational diabetic placentas and normal term placentas, total RNA preparations were evaluated qualitatively by northern blot and quantitatively by dot blot of RNA and cDNA hybridization to a nick-translated hPL-pMB9 plasmid. The northern blot revealed no major size differences of the mRNA and the dot blot hybridization was quantitatively similar for both gestational diabetics and normal terms per unit of total RNA. By direct analysis of DNA per g tissue we found the DNA content of placentas from gestational diabetics and normal term to be statistically the same.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparisons of human placental lactogen mRNA levels from placentas of diabetics and normal term. 397 53

A prospective study has been carried out of placental lactogen levels in pregnancy complicated by diabetes mellitus. The levels were higher than those in normal pregnant subjects; the higher levels were related to increased placental and fetal weight but more closely to the former; and lower levels were found when there was clinical evidence of placental dysfunction. Those patients requiring the largest insulin increment for the control of their diabetes in the pregnancy have placental lactogen levels in the higher range.
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PMID:Placental lactogen levels in diabetic pregnancy. 470 Mar 28

Both insulin and the related peptides, the insulin-like growth factors/somatomedins, may function as anabolic factors in the regulation of fetal body size. Infants born to women suffering from diabetes mellitus may show increased deposition of subcutaneous fat and enhanced lean body mass, findings reproduced in experimental animal fetuses with induced hyperinsulinaemia. Fetal adiposity may be associated with a life-time tendency to obesity and its associated diseases. Insulin-like growth factors I (IGFI) and II are present in the circulation of the newborn infant and animal fetus and correlate positively with birth size. The fetal tissues are biologically responsive to IGFs in vitro and are rich in specific cell membrane receptors, those predominantly recognizing IGFI being structurally and functionally similar to the insulin receptor. Insulin could theoretically influence fetal tissues by an interaction with either the insulin or IGF receptor. IGF release is a property of multiple fetal tissues in vitro, but, in contrast to postnatal life, is not dependent on growth hormone. Fetal IGF production may be influenced by placental lactogen, especially IGFII which rapidly declines in the circulation following parturition in the rat and sheep. A positive association also exists between circulating levels of insulin and IGFs when the former is experimentally manipulated in the animal fetus. Similarly the infant born with transient diabetes mellitus has low cord blood levels of insulin and IGFI. Insulin has a dual role in prenatal life. In the last trimester insulin functions as a glucoregulatory hormone, but from much earlier in gestation creates an anabolic environment in the fetus supplied with optimal nutrients. This latter mechanism of action is unclear and probably heterogeneous, but in overview is permissive rather than obligatory. In contrast the growth-promoting role of the IGFs is direct but their interaction with fetal tissues, and thus the overall emphasis of fetal growth, may be paracrine.
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PMID:Fetal growth control: the role of insulin and related peptides. 609 45

Serum human placental lactogen (hPL) and human chorionic gonadotropin (hCG) were assayed and fetal crown-rump length (CRL) was determined by sonar in three groups of pregnant women--35 with uncomplicated pregnancies, 13 with insulin-dependent diabetes mellitus, and 21 who represented a general pregnancy population. Each patient had a regular cycle and recorded last menstrual period, ovulated spontaneously, and was delivered of a single live baby. Serum hPL concentrations within the range 0.01-0.80 microU/ml in patients in the first group gave estimates of gestation with an SD of 6.3 days which was the same as the SD derived from CRL measurements. When the hPL regression equation was applied to the diabetic mothers the difference between the gestational age estimated from hPL and that estimated from LMP had a mean value of - 0.9 days with an SD of 6.2 days; this difference was not significantly different from zero. The third group of patients had a mean difference between hPL and LMP derived gestational age of 0.7 days (+/- 6.7 SD). Serum hPL offers a method of estimating gestation sufficiently precise to be used as a practical alternative to sonar measurements of CRL.
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PMID:Accurate assessment of early gestational age in normal and diabetic women by serum human placental lactogen concentration. 613 31


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