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

Glycogen content in the normal placenta decreases gradually towards term. However, in human diabetes and in rat streptozotocin diabetes two- to tenfold increases in placental glycogen level were found during the pregnancy. This elevation was evident in rats per tissue weight, protein or DNA content and was also seen in insulin-treated and gestational diabetics. Electron microscopic investigation of diabetic rat placenta revealed glycogen deposition in the typical glycogen cells, also in junctional zone cells and in all cells of the placental labyrinth. Placental glycogen accumulation in diabetes occurs in marked contrast to other tissues, such as maternal liver, from which glycogen disappears. Liver and muscle glycogenesis and glycogenolysis are under insulin control, by regulation of the activities of glycogen synthase and phosphorylase. However, in the placenta these enzymes are not meaningfully influenced by insulin in in vivo and in vitro studies. In our and other laboratories the activities of both enzymes somewhat increased or decreased, showing no trend conducive to glycogen accumulation. Placenta is glucose dependent, but the role of insulin in its carbohydrate metabolism is doubtful. Despite the high placental concentration of insulin receptors no metabolic outcome has yet been pointed out. Glycogen accumulation in the placenta of diabetic rats was found to be related to the extent of maternal hyperglycemia. The resultant markedly increased intracellular level of glucose-6-phosphate accelerates glycogen synthesis b. Glucose itself activates glycogen synthase and deactivates glycogen phosphorylase. Continuous glucose infusion to non-diabetic pregnant rats on gestation days 18-21 likewise also caused an increase in placental glycogen in correlation with hyperglycemia. The possibility that placental glycogen is under the control of fetal rather than maternal insulin was explored by producing insulin deficiency through intrafetal streptozotocin injection. There was no effect of fetal "diabetes" on placental glycogen synthesis or on the distribution of placental glycogen between the maternal and fetal segments of the placenta, while it caused a marked decrease in the fetal liver glycogen content and fetal body weight. To assess the availability of placental glycogen as an energy source the placental glycogenolysis was investigated after hormonal stimulation. Catecholamines were effective in inducing lactate formation both in vivo and in vitro in nondiabetic and diabetic rats. Protracted activation of the adenylate cyclase system by cholera toxin administration pronouncedly reduced placental glycogen in vivo.
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PMID:Placental glycogen metabolism in diabetic pregnancy. 183 20

Since glycogen accumulates in the placenta in diabetes and does not appear to be susceptible, in general, to the effect of fasting, the capacity of catecholamines to elicit glycogenolysis was investigated in non-diabetic and diabetic rats. Injection of epinephrine or isoproterenol caused a decrease in placental glycogen within 20 min in non-diabetic, 20 day pregnant rats, in association with the rise in serum glucose and lactate. Incubation with isoproterenol induced glycogenolysis in placental slices from non-diabetic and diabetic rats, nearly commensurate with lactate production. This effect of isoproterenol was concentration dependent and of similar magnitude in non-diabetic and diabetic rat placentas. Glucagon was ineffective in inducing placental glycogenolysis in vivo or in vitro. Protracted stimulation of the catecholamine receptor by the administration of cholera toxin effected a pronounced decrease in placental glycogen, percentagewise higher in diabetic than non-diabetic rats. These results show that placental glycogen is amenable to mobilization by hormonal stimuli effecting phosphorylase activation.
Placenta
PMID:Mobilization of placental glycogen in diabetic rats. 214 54

The placenta from 30 women with diabetes mellitus were examined and weighed at delivery. Nineteen of these were from women with overt and eleven from women with gestational diabetes. Eleven placentae from normal pregnancies served as controls. There was no difference between the mean +/- s.d. placental weight for the diabetic group and the control group (609 +/- 148 versus 591 +/- 93 g, NS). The mean placental weight ratios for the diabetic group and the control group were also similar (0.98 +/- 0.23 versus 0.89 +/- 0.15, NS). Moreover, there was no difference between the weights and weight ratios of placentae from women with overt (622 +/- 173 g, 1.02 +/- 0.27) and those with gestational diabetes (586 +/- 90 g, versus 0.90 +/- 0.13). Placental weights correlated with birthweights (r = 0.70, P less than 0.01) and with skinfold thickness measurements fo the infants (r = 0.40, P less than 0.05), but neither with gestational ages (r = 0.15, NS) nor with maternal glycosylated haemoglobin levels in the third trimester (r = 0.24, NS). Among the women with overt diabetes, placental weights were greater in those in White's class B and C than those in class D and R (689 +/- 143 versus 530 +/- 177 g; P less than 0.05). In general, placentae from well controlled diabetic patients were not heavier than those from normal pregnant women, although there was an increase in placental weight in White's class B and C, as compared with those in class D and R.
Placenta
PMID:Placental weight in diabetic pregnancies. 277 97

Although many studies in animal models and in cell cultures have shown that vanadate has insulin-like effects, it has not been studied in human diabetes mellitus. In this study the levels of vanadium in human placentae from 23 pregnancies complicated by gestational diabetes mellitus were compared with 18 uncomplicated non-diabetic pregnancies closely matched for maternal age, gravidity, and gestational age. Using the unpaired Student's t-test, the mid-disc placental levels in gestational diabetes (7.62 +/- 1.29 micrograms/g dry weight) were significantly lower (p less than 0.05) than controls (8.73 +/- 1.85 micrograms/g dry weight). These findings appear to be independent of placental size and birthweight. When these data were analyzed according to treatment, the vanadium levels in insulin-treated cases (8.07 +/- 1.32 micrograms/g dry weight) were not significantly different from the matched controls (8.84 +/- 1.69 micrograms/dry weight); the levels in noninsulin treated cases (7.08 +/- 1.25 micrograms/g dry weight), however, were significantly (p less than 0.005) lower than controls (8.99 +/- 1.96 micrograms/g dry weight). It is interesting to speculate that there may be increased binding of vanadium to maternal tissues in human diabetes mellitus when insulin is deficient.
Placenta
PMID:Placental vanadium in gestational diabetes mellitus. 278 May 18

Human placental villi from normal and pathological material from the eighth to the 40th week of gestation were examined by light, scanning and transmission electron microscopy. Trophoblastic specializations--such as syncytial sprouts of early and late pregnancy, syncytial knots and syncytial bridges--were classified into proliferative and degenerative processes or artefacts caused by tangential sectioning. In early pregnancy and in diabetes mellitus most syncytial sprouts represent the initial phases in the development of villi. In late pregnancy, in particular in pre-eclampsia, most syncytial knots, sprouts and bridges are histological artefacts, caused by tangential sectioning of the trophoblastic surface. The chance of producing such artefacts is increased with increasing section thickness and with increasing branching and tortuosity of the villi. However, a small proportion of the syncytial knots, sprouts and bridges in the last-trimester placenta, those containing coarse pyknotic nuclei, are trophoblastic specializations of a probably degenerative character.
Placenta
PMID:Interpretation of syncytial sprouts and bridges in the human placenta. 330 29

In an attempt to define better the metabolic differences between normal, insulin-dependent and non-insulin-dependent diabetes, we have compared the effect of insulin on the secretion of oestradiol and progesterone in term placental explant culture. Placentae from non-diabetic and from diabetic, non-insulin-dependent diabetic patients demonstrated a similar response to incubation with insulin. This response consisted of a dose-dependent increase in both oestradiol and progesterone in the incubation media after 24 h. In contrast, the placentae of insulin-dependent diabetics showed a decrease in oestradiol and no change in progesterone secretion following exposure to insulin. These differences in response to insulin may underlie other metabolic differences between the placentae in the different groups.
Placenta
PMID:The effect of insulin on oestradiol and progesterone release by normal and diabetic placentae in vitro. 331 91

Changes in the basement membranes associated with the placenta and fetal membranes have been observed in diabetic women, but little is known about the underlying alterations at the biochemical level. Present studies are concerned with the amount, chain composition and carbohydrate content of the collagens from amniotic membranes of women with overt and gestational diabetes. Collagens were obtained from these membranes using pepsin digestion and differential salt precipitation. In comparison with controls, the amounts of the interstitial and type IV collagens remained unchanged while the type V samples showed a moderate increase. However, by the use of reduced pepsinization, a fraction containing primarily type VII collagen and some type VI showed a significant increase in the tissues from diabetics, especially those from overt patients. Slab gel electrophoresis of the latter fractions revealed increased amounts of type VII collagen chains. The collagens from diabetics showed only small and marginally significant increases in their carbohydrate content. These observations suggest that changes in the 'intermediate' collagens as a group may play a role in the connective tissue changes associated with diabetes.
Placenta
PMID:Analysis of the collagens from the fetal membranes of diabetic mothers. 370 34

Pregnancy-associated plasma protein-A was assayed in the blood of 347 women during pregnancy, using a new primary standard of PAPP-A as reference. The protein was assayed by antibody-antigen crossed electrophoresis with the lower limit of confident assay being 9.5 micrograms PAPP-A/ml (13 pmol/ml). PAPP-A was first detected at 14 weeks of gestation; by term it had risen to within the range 20 to 320 micrograms/ml. There was an indication that pregnancies involving a male baby had higher PAPP-A levels in blood than did those involving female babies. In 51 blood samples from 30 patients with gestational diabetes (taken between 28 weeks of pregnancy and term) there was no significant alteration in PAPP-A values compared with controls. In 35 blood samples from 15 patients with insulin-dependent diabetes, levels of PAPP-A were significantly lower than in controls or in gestational diabetes. In 43 blood samples from 35 patients with babies affected with intrauterine growth retardation (between 28 weeks and term), there was no significant difference in PAPP-A levels compared with controls. The effect of insulin on the blood levels of PAPP-A suggests that the concentration of PAPP-A is capable of altering significantly in response to certain physiological changes associated with the control of carbohydrate metabolism.
Placenta
PMID:Studies on the concentration of pregnancy-associated plasma protein-A during normal and complicated pregnancy. 617 90

Full-term placentae of rats with streptozotocin-induced diabetes were analysed histochemically and biochemically for changes in mucopolysaccharide content. The experimental diabetes induced severe cystic degeneration in the spongiosa zone of the placenta and this was accompanied by extracellular deposition of hyaluronate and neutral polysaccharides. The labyrinth zone was affected to a lesser extent. Biochemical analysis also revealed quantitative differences in the total contents of mucopolysaccharides (MPS) between the two zones of the placenta in both diabetic and normal placentae. The spongiosa had a higher total mucopolysaccharide content than the labyrinth. Polysaccharides of low molecular weight were always predominant. The amount of hyaluronate exceeded the quantitites of sulphated mucopolysaccharides which were found in relatively small amounts in both placental zones. In diabetic placentae there was a two- to threefold increase, which was more pronounced in the spongiosa. The increase was observed among all types of MPS. A close correlation between the accumulation of MPS in the placenta and the degree of maternal hyperglycaemia was found. The placentae of the three streptozotocin-resistant animals showed neither histological nor biochemical changes. It is suggested that the accumulation of MPS in the diabetic placenta might be a consequence of a shift in carbohydrate metabolism induced by hyperglycaemia or a persistence of the fetal metabolic features as a part of a retarded maturational process of the placenta.
Placenta
PMID:Histochemical and quantitative biochemical changes in mucopolysaccharides of the term placenta of the diabetic rat. 621 Sep 4

After an electrically induced pseudopregnancy in rats in which deciduomas were produced by an intraluminal oil injection, the decidual tissue was studied morphologically on days 7, 10 and 13. A constant and dynamic wave of mitotic figures was found, which started on day 7 in the antimesometrial decidua, moving to the mesometrial decidua on day 10 and finally to the mesometrial triangle area on day 13 of pseudopregnancy. This and other morphological changes were compared with those found in pseudopregnant rats with streptozotocin-induced diabetes. On days 7 and 10 the incidence and distribution of mitotic figures were practically identical in both groups and statistically no significant difference was found in the uterine weight between the two groups on these two days. On day 13, two statistically significant differences were observed in the diabetic group: a fall in the uterine weight and a fall in the incidence of mitotic figures in the mesometrial triangle decidual cells. Associated with decidualization, a series of histological changes were studied in the arteries of the mesometrial triangle. Although the difference was not statistically significant, changes seemed to occur to a lesser degree in the diabetic group. It is concluded that the diabetic state has no influence in the early decidualization period, but it does have influence late in pseudopregnancy: a fall in the mitotic activity in the decidual tissue, a fall in the uterine weight and a less marked change in the spiral arteries which during pregnancy would supply the developing placenta with maternal blood.
Placenta
PMID:Decidual changes in the endometrium and morphological adaptation of the associated supplying arteries in the normal and diabetic pseudopregnant rat. 650 59


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