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Histopathological placental lesions in mild gestational hyperglycemic and diabetic women
Marilza VC Rudge, César P Lima, Débora C Damasceno, Yuri K Sinzato, Gustavo Napoli, Cibele VC Rudge, Franciane Q Gallego, Iracema MP Calderon
Diabetology & Metabolic Syndrome , 2011, DOI: 10.1186/1758-5996-3-19
Abstract: One-hundred-and-thirty-one placental samples were collected from Diabetes mellitus (DM) positive screened patients. Two diagnostic tests, glycemic profile and 100 g oral glucose tolerance test (OGTT) in parallel identified 4 groups normoglycemic, mild gestational hyperglycemia (MGH), gestational DM (GDM) or overt DM (DM). Placental tissue specimens and sections from 4 groups were obtained by uniform random sampling and stained with hematoxylin-eosin.Placentas from MGH group presented 17 types of histopathological change and higher rates of syncytial nodes and endarteritis. GDM placentas presented only nine types of histopathological change, high rates of dysmaturity, low rates of calcification and no syncytial nodes. Overt DM placentas showed 22 types of histopathological change, 21 of which were present in the preterm period. There were histopathological similarities between MGH and DM placentas, but the former exhibited a higher incidence of endarteritis, which has been described as a "post-mortem" phenomenon.Our results confirmed that the distinct placental changes associated with DM and MGH depend on gestational period during which the diabetic insult occurs. It may reasonably be inferred that subclinical maternal hyperglycemia during pregnancy, as showed in MGH group, is responsible for increased placental endarteritis, a postmortem lesion in the live fetus.The placenta is a maternal-fetal organ that separates the maternal and fetal circulations and plays a central metabolic role in pregnancy. The placenta of diabetic women has attracted much interest, primarily because it is thought that placental damage may be partially responsible for the high incidence of fetal complications in pregnancies complicated by Diabetes mellitus [1]. Glucose is the main nutrient that passes to the fetus by facilitated diffusion. Thus, increased amounts of glucose may reach the fetus by facilitated transport through the placenta [2]. Therefore, adaptations in cells that are in cont
Neonatally Induced Mild Diabetes in Rats and Its Effect on Maternal, Placental, and Fetal Parameters  [PDF]
Yuri Karen Sinzato,Gustavo Tadeu Volpato,Isabela Lovizutto Iessi,Aline Bueno,Iracema de Mattos Paranhos Calderon,Marilza Vieira Cunha Rudge,Débora Cristina Damasceno
Experimental Diabetes Research , 2012, DOI: 10.1155/2012/108163
Abstract: The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100 mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women.
Neonatally Induced Mild Diabetes in Rats and Its Effect on Maternal, Placental, and Fetal Parameters  [PDF]
Yuri Karen Sinzato,Gustavo Tadeu Volpato,Isabela Lovizutto Iessi,Aline Bueno,Iracema de Mattos Paranhos Calderon,Marilza Vieira Cunha Rudge,Débora Cristina Damasceno
Journal of Diabetes Research , 2012, DOI: 10.1155/2012/108163
Abstract: The aim of this study was to assess placental changes and reproductive outcomes in neonatally induced mild diabetic dams and fetal development in their offspring. At birth, female rats were assigned either to control or diabetic group (100?mg of streptozotocin/Kg, subcutaneously). At adulthood, the female rats were mated. During pregnancy, the blood glucose levels and glucose and insulin tolerance tests were performed. At term, maternal reproductive outcomes, fetal and placental weight, and placental morphology were analyzed. Diabetic rats had smaller number of living fetuses, implantations and corpora lutea, and increased rate of embryonic loss. Placenta showed morphometric alterations in decidua area. Our results showed that mild diabetes was sufficient to trigger alterations in maternal organism leading to impaired decidua development contributing to failure in embryonic implantation and early embryonic losses. Regardless placental decidua alteration, the labyrinth, which is responsible for the maternal-fetal exchanges, showed no morphometric changes contributing to an appropriate fetal development, which was able to maintain normal fetal weight at term in mild diabetic rats. Thus, this experimental model of diabetes induction at the day of birth was more effective to reproduce the reproductive alterations of diabetic women. 1. Background Pregnant women with type 1 or type 2 diabetes are at increased risk of miscarriage, stillbirth, congenital malformations, placental abnormalities, and intrauterine malprogramming. Despite current treatments, maternal diabetes is an unfavorable environment for embryonic and fetoplacental development [1–7]. These important aspects of human diabetic pregnancies can be studied using the appropriate animal models [8], not only by ethical reasons but also by the multiplicity of uncontrolled variables that may modify the intrauterine environment [9]. Experimental models of severe diabetes (glycemia > 300?mg/dL), which reproduce the clinical conditions of poorly controlled type-1 diabetes, have been widely used [10–14]. However, only a few studies have evaluated the repercussions of diabetes on pregnant rats and/or their offspring [9, 15–18] using models of mild diabetes (glycemia between 120 and 300?mg/dL). In a previous study conducted at our laboratory [19], experimental mild diabetes induced at 5 days of life was not effective in reproducing the reproductive outcomes (miscarriage, fetal viability, and morbidity) observed in diabetic pregnant women. Although glycemic levels were consistent with those reported elsewhere,
Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat  [cached]
Emin Türkay Korgun,Nuray Acar,Leyla Sati,Dijle Kipmen-Korgun
Folia Histochemica et Cytobiologica , 2011, DOI: 10.5603/4131
Abstract: In various tissues, glucocorticoids (GCs) are known to downregulate glucose transport systems; however, their effects on glucose transporters (GLUTs) in the placenta of a diabetic rat are unknown. Glucocorticoid hormone action within the cell is regulated by the glucocorticoid receptor (GR). Thus, this study was designed to investigate the relationship between GR and glucose transporter expression in the placenta of the diabetic rat. Our immunohistochemical results indicated that GR and glucose transporter protein 1 (GLUT 1) are expressed ubiquitously in the trophoblast and endothelial cells of the labyrinthine zone, where maternal fetal transport takes place in the rat placenta. Expression of GR in the junctional zone of the rat placenta was detected in giant cells, and in some spongiotrophoblast cells, but not in the glycogen cells. GLUT 1 was present, especially in glycogen cells during early pregnancy, and in the spongiotrophoblast cells of the junctional zone during late pregnancy. Amounts of GR and GLUT 1 protein were increased towards the end of gestation both in the control and the diabetic placenta. However, at days 17 and 19 of gestation, only the placental GR protein was significantly increased in the streptozotocin-induced diabetic rats compared to control rats. Diabetes led to a significant decrease in placental weight at gestation day 15. In contrast, at gestational days 17 and 21, the weights of the diabetic placenta were significantly increased as compared with the controls. Moreover, diabetes induced fetus intrauterine growth retardation at gestational days 13, 17 and 21. In conclusion, the localization pattern of GR and GLUT 1 proteins in the same cell types led us to believe that there might be a relationship between GR and GLUT 1 expressions at the cellular level. GLUT 1 does not play a pivotal role in diabetic pregnancies. However, placental growth abnormalities during diabetic pregnancy may be related to the amount of GR. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 2, pp. 325–334)
Partial recovery of erythrocyte glycogen in diabetic rats treated with phenobarbital
Brazilian Journal of Medical and Biological Research , 1997, DOI: 10.1590/S0100-879X1997000500014
Abstract: erythrocytes may play a role in glucose homeostasis during the postprandial period. erythrocytes from diabetic patients are defective in glucose transport and metabolism, functions that may affect glycogen storage. phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (niddm), increasing the insulin-mediated glucose disposal. we studied the effects of phenobarbital treatment in vivo on glycemia and erythrocyte glycogen content in control and alloxan-diabetic rats during the postprandial period. in control rats (blood glucose, 73 to 111 mg/dl in femoral and suprahepatic veins) the erythrocyte glycogen content was 45.4 ± 1.1 and 39.1 ± 0.8 μg/g hb (mean ± sem, n = 4-6) in the femoral artery and vein, respectively, and 37.9 ± 1.1 in the portal vein and 47.5 ± 0.9 in the suprahepatic vein. diabetic rats (blood glucose, 300-350 mg/dl) presented low (p<0.05) erythrocyte glycogen content, i.e., 9.6 ± 0.1 and 7.1 ± 0.7 μg/g hb in the femoral artery and vein, respectively, and 10.0 ± 0.7 and 10.7 ± 0.5 in the portal and suprahepatic veins, respectively. after 10 days of treatment, phenobarbital (0.5 mg/ml in the drinking water) did not change blood glucose or erythrocyte glycogen content in control rats. in diabetic rats, however, it lowered (p<0.05) blood glucose in the femoral artery (from 305 ± 18 to 204 ± 45 mg/dl) and femoral vein (from 300 ± 11 to 174 ± 48 mg/dl) and suprahepatic vein (from 350 ± 10 to 174 ± 42 mg/dl), but the reduction was not sufficient for complete recovery. phenobarbital also stimulated the glycogen synthesis, leading to a partial recovery of glycogen stores in erythrocytes. in treated rats, erythrocyte glycogen content increased to 20.7 ± 3.8 μg/g hb in the femoral artery and 30.9 ± 0.9 μg/g hb in the suprahepatic vein (p<0.05). these data indicate that phenobarbital activated some of the insulin-stimulated glucose metabolism steps which were depressed in diabetic erythrocy
Partial recovery of erythrocyte glycogen in diabetic rats treated with phenobarbital  [cached]
da-Silva C.A.,Gon?alves A.A.
Brazilian Journal of Medical and Biological Research , 1997,
Abstract: Erythrocytes may play a role in glucose homeostasis during the postprandial period. Erythrocytes from diabetic patients are defective in glucose transport and metabolism, functions that may affect glycogen storage. Phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (NIDDM), increasing the insulin-mediated glucose disposal. We studied the effects of phenobarbital treatment in vivo on glycemia and erythrocyte glycogen content in control and alloxan-diabetic rats during the postprandial period. In control rats (blood glucose, 73 to 111 mg/dl in femoral and suprahepatic veins) the erythrocyte glycogen content was 45.4 ± 1.1 and 39.1 ± 0.8 μg/g Hb (mean ± SEM, N = 4-6) in the femoral artery and vein, respectively, and 37.9 ± 1.1 in the portal vein and 47.5 ± 0.9 in the suprahepatic vein. Diabetic rats (blood glucose, 300-350 mg/dl) presented low (P<0.05) erythrocyte glycogen content, i.e., 9.6 ± 0.1 and 7.1 ± 0.7 μg/g Hb in the femoral artery and vein, respectively, and 10.0 ± 0.7 and 10.7 ± 0.5 in the portal and suprahepatic veins, respectively. After 10 days of treatment, phenobarbital (0.5 mg/ml in the drinking water) did not change blood glucose or erythrocyte glycogen content in control rats. In diabetic rats, however, it lowered (P<0.05) blood glucose in the femoral artery (from 305 ± 18 to 204 ± 45 mg/dl) and femoral vein (from 300 ± 11 to 174 ± 48 mg/dl) and suprahepatic vein (from 350 ± 10 to 174 ± 42 mg/dl), but the reduction was not sufficient for complete recovery. Phenobarbital also stimulated the glycogen synthesis, leading to a partial recovery of glycogen stores in erythrocytes. In treated rats, erythrocyte glycogen content increased to 20.7 ± 3.8 μg/g Hb in the femoral artery and 30.9 ± 0.9 μg/g Hb in the suprahepatic vein (P<0.05). These data indicate that phenobarbital activated some of the insulin-stimulated glucose metabolism steps which were depressed in diabetic erythrocytes, supporting the view that erythrocytes participate in glucose homeostasis
Neonatally induced diabetes: liver glycogen storage in pregnant rats
Iessi, Isabela Lovizutto;Bueno, Aline;Sinzato, Yuri Karen;Spada, Ana Paula Machado;Rudge, Marilza Vieira Cunha;Heubel, Maricê Thereza Correa Domingues;Damasceno, Débora Cristina;
Brazilian Archives of Biology and Technology , 2012, DOI: 10.1590/S1516-89132012000200010
Abstract: the aim of this sstudy was to evaluate the liver glycogen storage in pregnant rats presenting neonatal streptozotocin-induced diabetes and to establish a relation with glycemia and insulin levels. wistar rats were divided in to two groups: 1) mild diabetes (stz) - received streptozotocin (glycemia from 120 to 300 mg/dl), 2) control - received vehicle (glycemia below 120 mg/dl). at days 0, 7, 14 and 21 of the pregnancy, body weight and glycemia were evaluated. at day 21 of the pregnancy, the rats were anesthetized for blood and liver collection so as to determine insulin and liver glycogen, which showed no changes in the stz group as compared to the controls. in the stz group, maternal weight gain were lower as compared to those in the control group. significantly increased glycemia was observed at days 0 and 14 of the pregnancy in the stz group. therefore, neonatally induced diabetes in the rats did not cause metabolic changes that impaired insulin and liver glycogen relation in these rats.
Plasma concentrations and placental immunostaining of interleukin-10 and tumornecrosis factor-α as predictors of alterations in the embryo-fetal organism and the placental development of diabetic rats
Sinzato, Y.K.;Damasceno, D.C.;Laufer-Amorim, R.;Rodrigues, M.M.P.;Oshiiwa, M.;Taylor, K.N.;Rudge, M.V.C.;
Brazilian Journal of Medical and Biological Research , 2011, DOI: 10.1590/S0100-879X2011007500015
Abstract: interleukin-10 (il-10) appears to be the key cytokine for the maintenance of pregnancy and inhibits the secretion of inflammatory cytokines such as tumor necrosis factor-α (tnf-α). however, there are no studies evaluating the profile of these cytokines in diabetic rat models. thus, our aim was to analyze il-10 and tnf-α immunostaining in placental tissue and their respective concentrations in maternal plasma during pregnancy in diabetic rats in order to determine whether these cytokines can be used as predictors of alterations in the embryo-fetal organism and in placental development. these parameters were evaluated in non-diabetic (control; n = 15) and wistar rats with streptozotocin (stz)-induced diabetes (n = 15). at term, the dams (100 days of life) were killed under anesthesia and plasma and placental samples were collected for il-10 and tnf-α determinations by elisa and immunohistochemistry, respectively. the reproductive performance was analyzed. plasma il-10 concentrations were reduced in stz rats compared to controls (7.6 ± 4.5 vs 20.9 ± 8.1 pg/ml). the placental scores of immunostaining intensity did not differ between groups (p > 0.05). prevalence analysis showed that the il-10 expression followed tnf-α expression, showing a balance between them. stz rats also presented impaired reproductive performance and reduced plasma il-10 levels related to damage during early embryonic development. however, the increased placental il-10 as a compensatory mechanism for the deficit of maternal regulation permitted embryo development. therefore, the data suggest that il-10 can be used as a predictor of changes in the embryo-fetal organism and in placental development in pregnant diabetic rats.
Placental Transfer of Lactate, Glucose and 2-deoxyglucose in Control and Diabetic Wistar Rats  [PDF]
Chris R. Thomas,Beryl B. Oon,Clara Lowy
Experimental Diabetes Research , 2001, DOI: 10.1155/edr.2001.113
Abstract: Placental transfer of lactate, glucose and 2-deoxyglucose was examined employing the in situ perfused placenta. Control and streptozotocin induced diabetic Wistar rats were infused with [U-C14]-glucose and [H3]-2-deoxyglucose (2DG). The fetal side of the placenta was perfuseci with a cell free medium and glucose uptake was calculated in the adjacent fetuses. Despite the 5-fold higher maternal plasma glucose concentration in the diabetic dams the calculated fetal glucose metabolic index was not significantly different between the 2 groups. Placental blood flow was reduced in the diabetic animals compared with controls but reduction of transfer of [U-C14]-glucose and [H3]-2-deoxyglucose and endogenously derived [C14]-Lactate to the fetal compartment, could not be accounted for by reduced placental blood flow alone. There was no significant net production or uptake of lactate into the perfusion medium that had perfused the fetal side of the placenta in either group. The plasma lactate levels in the fetuses adjacent to the perfused placenta were found to be higher than in the maternal plasma and significantly higher in the fetuses of the diabetic group compared with control group. In this model the in situ perfused placenta does not secrete significant quantities of lactate into the fetal compartment in either the control or diabetic group.
Chronic Treatment with the AMP-Kinase Activator AICAR Increases Glycogen Storage and Fatty Acid Oxidation in Skeletal Muscles but Does Not Reduce Hyperglucagonemia and Hyperglycemia in Insulin Deficient Rats  [PDF]
Kaio F. Vitzel, George Bikopoulos, Steven Hung, Kathryn E. Pistor, Jessica D. Patterson, Rui Curi, Rolando B. Ceddia
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0062190
Abstract: This study tested whether the glycogen-accumulating effect of chronic in vivo pharmacological 5′AMP-activated protein kinase (AMPK) activation could improve glycemic control under conditions of insulin deficiency. Male Wistar rats were rendered diabetic through the administration of streptozotocin (STZ) and then treated for 7 consecutive days with the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-rib?ofuranoside(AICAR). Subsequently, glycogen content and synthesis, glucose oxidation, and fatty acid oxidation (FAO) were determined in oxidative and glycolytic skeletal muscles. Glycemia, insulinemia, glucagonemia, and circulating triglycerides (TG) and non-esterified fatty acids (NEFAs) were measured after AICAR treatment. Insulin was almost undetectable in STZ rats and these animals were severely hyperglycemic. Glycogen content was markedly low mainly in glycolytic muscles of STZ rats and AICAR treatment restored it to control values. No differences were found among all muscles studied with regards to the content and phosphorylation of Akt/protein kinase B and glycogen synthase kinase 3. Even though glycogen synthase content was reduced in all muscles from STZ rats, insulin-induced dephosphorylation/activation of this enzyme was preserved and unaffected by AICAR treatment. Glucagon and NEFAS were 2- and 7.4-fold fold higher in STZ rats than controls, respectively. AICAR did not affect hyperglycemia and hyperglucagonemia in STZ rats; however, it normalized circulating NEFAs and significantly increased FAO in glycolytic muscles. In conclusion, even though AICAR-induced AMPK activation enhanced glycogen accumulation in glycolytic muscles and normalized circulating NEFAs and TG levels, the hyperglycemic effects of glucagon likely offset the potentially glucose-lowering effects of AICAR, resulting in no improvement of glycemic control in insulin-deficient rats.
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