Diabetic Pregnant Rats Research Articles

Anti-hyperglycemic effects of three medicinal plants in diabetic pregnancy: modulation of T cell proliferation

BackgroundPopulations in Africa mostly rely on herbal concoctions for their primarily health care, but so far scientific studies supporting the use of plants in traditional medicine remain poor. The present study was undertaken to evaluate the anti-hyperglycemic effects of Picralima nitida (seeds), Nauclea latifolia (root and stem) and Oxytenanthera abyssinica (leaves) commonly used, in diabetic pregnancy.MethodsPregnant wistar rats, rendered diabetic by multiple low injections of streptozotocin, were treated with selected plant extracts based on their antioxidant activities. Vitamin C concentrations, fatty acid compositions and phytochemical analysis of plants extracts were determined. Effect of selected plant extracts on human T cell proliferation was also analysed.ResultsAll analysed plant extracts exhibited substantial antioxidant activities probably related to their content in polyphenols. Picralima nitida exhibited the highest antioxidant capacity. Ethanolic and butanolic extracts of Picralima nitida, butanolic extract of Nauclea latifolia and ethanolic extract of Oxytenanthera abyssinica significantly decreased hyperglycemia in the diabetic pregnant rats. Butanolic extract of Picralima, also appeared to be the most potent immunosuppressor although all of the analysed extracts exerted an immunosuppressive effect on T cell proliferation probably due to their linolenic acid (C18:3n-3) and/or alkaloids content. Nevertheless, all analysed plants seemed to be good source of saturated and monounsaturated fatty acids.ConclusionBy having antioxidant, anti-hyperglycemic and immunosuppressive activities, these plants could be good candidates in the treatment of diabetes and diabetic pregnancy.

Role of impaired endothelial cell Ca2+signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy

Diabetes mellitus in pregnancy is associated with impaired endothelium-mediated dilatation of maternal arteries, although the underlying cellular mechanisms remain unknown. In this study, we hypothesized that diabetes during rat gestation attenuates agonist-induced uterine vasodilation through reduced endothelial cell (EC) Ca(2+) elevations and impaired smooth muscle cell (SMC) hyperpolarization and SMC intracellular Ca(2+) concentration ([Ca(2+)]i) responses. Diabetes was induced by an injection of streptozotocin to second-day pregnant rats and confirmed by the development of maternal hyperglycemia. Control rats were injected with a citrate buffer. Fura-2-based measurements of SMC [Ca(2+)]i or microelectrode recordings of SMC membrane potential were performed concurrently with dilator responses to ACh in uteroplacental arteries from control and diabetic pregnant rats. Basal levels of EC [Ca(2+)]i and ACh-induced EC [Ca(2+)]i elevations in pressurized vessels and small EC sheets were studied as well. Diabetes reduced ACh-induced vasodilation due to a markedly impaired EDHF-mediated response. Diminished vasodilation to ACh was associated with attenuated SMC hyperpolarization and [Ca(2+)]i responses. Basal levels of EC [Ca(2+)]i and ACh-induced EC [Ca(2+)]i elevations were significantly reduced by diabetes. In conclusion, these data demonstrate that reduced endothelium-mediated hyperpolarization contributes to attenuated uteroplacental vasodilation and SMC [Ca(2+)]i responses to ACh in diabetic pregnancy. Impaired endothelial Ca(2+) signaling is in part responsible for endothelial dysfunction in the uterine resistance vasculature of diabetic rats. Pharmacological improvement of EC Ca(2+) handling may provide an important strategy for the restoration of endothelial function and enhancement of maternal blood flow in human pregnancies complicated by diabetes.

Influence of treatment with quercetin on lipid parameters and oxidative stress of pregnant diabetic rats

Among the numerous coadjuvant therapies that could influence the incidence and progression of diabetic complications, antioxidants and flavonoids are currently being tested in clinical trials. We investigated the effect of quercetin on biochemical parameters in streptozotocin-induced (60 mg/kg body mass, by intraperitoneal injection) diabetic rats. A total of 32 female Wistar rats were distributed among 4 groups as follows: control (G1); control treated with quercetin (G2); diabetic (G3); and diabetic treated with quercetin (G4). Quercetin administered to pregnant diabetic rats controlled dyslipidemia and improved lipid profiles in diabetes mellitus, regulated oxidative stress by reducing the generation of lipid hydroperoxides, and increased the activity of the antioxidant enzyme glutathione peroxidase.

Effect of oral supplementation of the linoleic and gammalinolenic acids on the diabetic pregnant rats

ABSTRACT The aim of this work was to evaluate the direct protective action of oral fatty acid supplementation against the deleterious effect of hyperglycemia on maternal reproductive outcomes; fetal growth and development on female Wistar rats. The animals were distributed into four experimental groups: G1= non-diabetic without supplementation (Control group); G2= non-diabetic treated with linoleic (LA) and gammalinolenic acid (GLA) (1 mL of Gamaline-V/day); G3= diabetic without supplementation and G4= diabetic treated with LA and GLA. Diabetes was induced by streptozotocin (40 mg/kg). At day 21 of pregnancy, the gravid uterus was weighed and dissected to count the dead and live fetuses, resorption, implantation, and corpora lutea numbers. The fetuses were analyzed for external and internal anomalies. The treatment with Gamaline-V supplementation to diabetic rats interfered in the maternal reproductive outcome (reduced number of live fetuses and embryonic implantation); however, it protected the deleterious on the incidence of congenital anomalies caused by hyperglycemia. Key words: diabetes, rat, pregnancy, anomalies, fatty acid supplementation, Gamaline-V

M246 HEAT SHOCK PROTEIN PRODUCTION AND IMMUNITY AND ALTERED FETAL DEVELOPMENT IN DIABETIC PREGNANT RATS

International Journal of Gynecology & ObstetricsVolume 119, Issue S3 p. S611-S611 Poster presentations M246 HEAT SHOCK PROTEIN PRODUCTION AND IMMUNITY AND ALTERED FETAL DEVELOPMENT IN DIABETIC PREGNANT RATS M.V.C. Rudge, M.V.C. RudgeSearch for more papers by this authorF.H. Saito, F.H. SaitoSearch for more papers by this authorD. Damasceno, D. DamascenoSearch for more papers by this authorI. Calderon, I. CalderonSearch for more papers by this authorI.L. lessi, I.L. lessiSearch for more papers by this authorA. Bueno, A. BuenoSearch for more papers by this authorS.B. Corvino, S.B. CorvinoSearch for more papers by this authorB. Dallaqua, B. DallaquaSearch for more papers by this authorG. Marini, G. MariniSearch for more papers by this authorF. Piculo, F. PiculoSearch for more papers by this authorS.S. Witkin, S.S. WitkinSearch for more papers by this author M.V.C. Rudge, M.V.C. RudgeSearch for more papers by this authorF.H. Saito, F.H. SaitoSearch for more papers by this authorD. Damasceno, D. DamascenoSearch for more papers by this authorI. Calderon, I. CalderonSearch for more papers by this authorI.L. lessi, I.L. lessiSearch for more papers by this authorA. Bueno, A. BuenoSearch for more papers by this authorS.B. Corvino, S.B. CorvinoSearch for more papers by this authorB. Dallaqua, B. DallaquaSearch for more papers by this authorG. Marini, G. MariniSearch for more papers by this authorF. Piculo, F. PiculoSearch for more papers by this authorS.S. Witkin, S.S. WitkinSearch for more papers by this author First published: 22 October 2012 https://doi.org/10.1016/S0020-7292(12)61438-6AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume119, IssueS3Abstracts of XX FIGO World Congress of Gynecology and ObstetricsOctober 2012Pages S611-S611 RelatedInformation

Treatment with Azadirachta indica in diabetic pregnant rats: Negative effects on maternal outcome

Ethnopharmacological relevanceThe role of Azadirachta indica (neem) against Chagas disease and its antibiotic and antidiabetic action have been demonstrated in non-pregnant animals. However, the effects of neem on lipid metabolism and oxidative stress during pregnancy remain to be investigated. The objective of this study was to evaluate the effects of Azadirachta indica (neem) on maternal reproductive performance and biochemical parameters in non-diabetic and streptozotocin-induced mild diabetic rats (MD). Materials and methodsPregnant rats were randomly distributed into six experimental groups: ND=non-treated non-diabetic (n=13); NDOil=non-diabetic treated with 1.2mL/day neem seed oil (n=12); NDPA=non-diabetic treated with 1.0mg/mL/day azadirachtin (n=12); D=non-treated diabetic (n=13); DOil: diabetic treated with neem seed oil (n=12), and DPA=diabetic treated with azadirachtin, n=13. Treatment with either neem oil (1.2mL/day) or azadirachtin (1.0mg/mL/day) was orally administered throughout pregnancy. Glucose test tolerance (GTT) was performed at day 17 of pregnancy and used as an inclusion criterion. At term pregnancy, maternal reproductive outcomes, lipid profile and oxidative stress status were assessed. ResultsTreatment with neem oil and azadirachtin during pregnancy (1) had no hypoglycemic and anti-hyperglycemic effects on non-diabetic and diabetic rats, respectively; (2) affected OGTT glycemic levels in diabetic rats; (3) increased the proportion of fetuses classified as small for pregnancy age (SPA) in all groups; and (4) did not interfere with the lipid profile in non-diabetic dams. Neem oil reduced the rate of total cholesterol and NEFA in diabetic animals. Both neem oil and azadirachtin increased lipoperoxidation, characterized by increased MDA levels in non-diabetic rats. ConclusionBoth neem seed oil and azadirachtin impaired intrauterine development and altered antioxidant/oxidative status during pregnancy.

Embryo Development and Macrophage Phenotype in Normal and Diabetic Rat Pregnancy.

Embryo Development and Macrophage Phenotype in Normal and Diabetic Rat Pregnancy.

Heat shock protein production and immunity and altered fetal development in diabetic pregnant rats

We evaluated associations between the concentrations of heat shock proteins (hsp60 and hsp70) and their respective antibodies, alterations in maternal reproductive performance, and fetal malformations in pregnant rats with hyperglycemia. Mild diabetes (MD) or severe diabetes (SD) was induced in Sprague-Dawley rats prior to mating; non-treated non-diabetic rats (ND) served as controls. On day 21 of pregnancy, maternal blood was analyzed for hsp60 and hsp70 and their antibodies; and fetuses were weighed and analyzed for congenital malformations. Hsp and anti-hsp levels were correlated with blood glucose levels during gestation. There was a positive correlation between hsp60 and hsp70 levels and the total number of malformations (R = 0.5908, P = 0.0024; R = 0.4877, P = 0.0134, respectively) and the number of malformations per fetus (R = 0.6103, P = 0.0015; R = 0.4875, P = 0.0134, respectively). The anti-hsp60 IgG concentration was correlated with the number of malformations per fetus (R = 0.3887, P = 0.0451) and the anti-hsp70 IgG level correlated with the total number of malformations (R = 0.3999, P = 0.0387). Moreover, both hsp and anti-hsp antibodies showed negative correlations with fetal weight. The results suggest that there is a relationship between hsp60 and hsp70 levels and their respective antibodies and alterations in maternal reproductive performance and impaired fetal development and growth in pregnancies associated with diabetes.

Coexistence of insulin resistance and increased glucose tolerance in pregnant rats: A physiological mechanism for glucose maintenance

AimThe contribution of insulin resistance (IR) and glucose tolerance to the maintenance of blood glucose levels in non diabetic pregnant Wistar rats (PWR) was investigated. Main methodsPWR were submitted to conventional insulin tolerance test (ITT) and glucose tolerance test (GTT) using blood sample collected 0, 10 and 60min after intraperitoneal insulin (1U/kg) or oral (gavage) glucose (1g/kg) administration. Moreover, ITT, GTT and the kinetics of glucose concentration changes in the fed and fasted states were evaluated with a real-time continuous glucose monitoring system (RT-CGMS) technique. Furthermore, the contribution of the liver glucose production was investigated. Key findingsConventional ITT and GTT at 0, 7, 14 and 20days of pregnancy revealed increased IR and glucose tolerance after 20days of pregnancy. Thus, this period of pregnancy was used to investigate the kinetics of glucose changes with the RT-CGMS technique. PWR (day 20) exhibited a lower (p<0.05) glucose concentration in the fed state. In addition, we observed IR and increased glucose tolerance in the fed state (PWR-day 20 vs. day 0). Furthermore, our data from glycogenolysis and gluconeogenesis suggested that the liver glucose production did not contribute to these changes in insulin sensitivity and/or glucose tolerance during late pregnancy. SignificanceIn contrast to the general view that IR is a pathological process associated with gestational diabetes, a certain degree of IR may represent an important physiological mechanism for blood glucose maintenance during fasting.

The causal role of PKC in Reduced Endothelial Ca2+ Signaling and Impaired EDHF‐Mediated Uterine Vasodilation in Diabetic Pregnancy

Increased PKC activity is an essential mechanism of diabetic vascular complications. To characterize the role of PKC in uterine vascular dysfunction during diabetic pregnancy we: (1) defined the effects of PKC activation (PDBu) or inhibition (bisindolylmaleimide, BIS) on EDHF‐mediated responses to ACh; (2) elucidated PKC dependence of ACh‐induced endothelial cell (EC) [Ca2+]i.Diabetes was induced by streptozotocin (STZ) injection. ACh was tested in uterine arteries from control and diabetic pregnant rats in the presence of L‐NNA and indomethacin. Fura‐2 based SMC or EC [Ca2+]i responses were studied as well. Diabetes reduced EDHF‐mediated vasodilation from 90 ± 4 % to 26 ± 9 % at 10 μM ACh. SMC and EC [Ca2+]i responses were markedly reduced as well. PDBu inhibited ACh‐evoked vasodilation (14 ± 5 %) and associated SMC [Ca2+]i responses of control vessels. BIS partially restored EDHF‐mediated vasodilation (to 72 ± 10 %) and SMC [Ca2+]i in diabetic vessels. PDBu reduced EC [Ca2+]i responses of control vessels to ACh by 50 ± 7 %. BIS significantly restored EC [Ca2+]i elevations to ACh in diabetic arteries.PKC‐dependent reduction in EC Ca2+ signaling underlies impaired EDHF‐mediated uterine vasodilation during diabetic pregnancy. Inhibition of PKC may serve as a therapeutic strategy to improve uterine vasodilation in pregnancies complicated with diabetes. Supported by NIH HL088245

Evaluation of cell proliferation and apoptosis in placentas of rats with severe diabetes

The aim of this work was to analyze the cell proliferation and apoptosis indexes on the 18th and 21st days of pregnancy of diabetic rats and to correlate with maternal glycemia and perinatal outcomes. Placentas from 20 Wistar rats were collected and divided into four experimental groups: control and diabetic of 18 and 21 days of pregnancy. The cell proliferation was analyzed using the PCNA expression and apoptosis by the TUNEL method. It was observed that PCNA and TUNEL indexes decreased from day 18 to 21 of pregnancy in the placentas of diabetic rats and these values were lower than control groups. Diabetic dams presented higher percentage of small for pregnancy age (SPA) fetuses. However, there was no difference between the PCNA and TUNEL indexes in SPA and N-SPA fetuses in all the groups and these indexes were not correlated to maternal glycemic. Thus, placental cell proliferation and apoptosis did not interfere in the intrauterine growth restriction.

Influence of maternal metabolism and parental genetics on fetal maldevelopment in diabetic rat pregnancy

The purpose of this study was to investigate the influence of parental transgenerational genetics and maternal metabolic state on fetal maldevelopment in diabetic rat pregnancy. Rats from an inbred malformation-resistant (W) strain, and an inbred malformation-prone (L) strain, were cross-mated to produce two different F(1) hybrids, WL and LW. Normal (N) and manifestly diabetic (MD) WL and LW females were mated with normal males of the same F(1) generation to obtain WLWL and LWLW F(2) hybrids. Maternal diabetes increased malformation and resorption rates in both F(2) generations. MD-WLWL offspring had higher resorption rate but similar malformation rate compared with the MD-LWLW offspring. Malformed MD-WLWL offspring presented with 100% agnathia/micrognathia, whereas malformed MD-LWL offspring had 60% agnathia/micrognathia and 40% cleft lip and palate. The MD-WL dams showed increased β-hydroxybutyrate levels and alterations in concentrations of several amino acids (taurine, asparagine, citrulline, cystine, glutamic acid, leucine, tyrosine, and tryptophan) compared with MD-LW dams. Fetal glyceraldehyde-3-phosphate dehydrogenase (Gapdh) activity and gene expression were more altered in MD-WLWL than MD-LWLW. Fetal gene expression of reactive oxygen species (ROS) scavenger enzymes was diminished in MD-WLWL compared with MD-LWLW. Glial cell line-derived neurotrophic factor and Ret proto-oncogene gene expression was decreased in both MD-WLWL and MD-LWLW fetuses, whereas increased bone morphogenetic protein 4 and decreased Sonic hedgehog homolog expression was found only in MD-LWLW fetuses. Despite identical autosomal genotypes, the WL and LW dams gave birth to offspring with markedly different malformation patterns. Together with fetal differences in enzymatic activity and expression of Gapdh, ROS scavengers, and developmental genes, these results may suggest a teratological mechanism in diabetic pregnancy influenced by maternal metabolism and parental strain epigenetics.

Taurine attenuates maternal and embryonic oxidative stress in a streptozotocin-diabetic rat model

Oxidative stress mechanisms have been implicated in congenital anomalies and morbidity/mortality of fetus/newborn in diabetic pregnancy. Numerous antioxidant treatments have shown varied beneficial effects in improving both maternal and fetal outcomes. The present study examined the propensity of taurine to attenuate the degree of embryopathy and oxidative stress among pregnant diabetic rats. Adult rats (CFT-Wistar) were rendered diabetic with an acute dose of streptozotocin (STZ; 45mg/kg bodyweight) on gestation day (GD) 4. Both Diabetic and non-diabetic dams were given oral supplements of taurine (0.5 and 1g/kg bodyweight/day) from GD 5 to GD 12. Maternal diet intake, bodyweight gain and urine output were monitored and dams were killed on GD 13. Markers of oxidative stress were determined in embryos and maternal livers. STZ treatment induced marked embryopathy (32%) and taurine supplements markedly reduced the degree of embryopathy (54% protection). The STZ-induced higher oxidative stress was significantly attenuated in rats given taurine supplements (P<0.05) and a similar effect was seen in embryos (P<0.05). These data suggest that dietary taurine during pregnancy provides significant protection against diabetes-induced oxidative stress in both the mother and the embryos and thus may serve as a therapeutic supplement during diabetic pregnancy.Diabetes during pregnancy affects >5% of all pregnancies, causing reproductive abnormalities that enhance spontaneous abortion – congenital anomalies, morbidity and mortality of both mother and fetus/newborn. One of the major mechanisms is increased oxidative stress caused by hyperglycaemia and the most prominent anti-teratogenic effect was achieved using antioxidative agents. Management of oxidative stress is considered, along with tight glycaemic control, to be beneficial both before conception and during pregnancy. Taurine, a ubiquitous amino acid found in almost all mammalian tissues, constitutes more than 50% of free amino acids. The aim of the study was to determine whether oral taurine supplementation given to pregnant diabetic rats during the post-implantation period could reduce embryo lethality and protect the developing embryos against maternal hyperglycaemia-induced oxidative stress. Adult rats were rendered diabetic with an acute dose of streptozotocin on gestation day (GD) 4. Both diabetic and non-diabetic dams were administered oral taurine for a period of 8days (GD 5–13). Maternal diet intake, bodyweight gain and urine output were monitored and dams were killed on GD 13. Markers of oxidative stress and antioxidant defences were studied in embryos and maternal livers. STZ induced marked embryopathy (32%) and taurine supplementation offered significant protection (54%). Taurine significantly offset diabetes-associated oxidative stress in the embryos of diabetic rats. These data suggest that dietary taurine supplementation during pregnancy provides significant protection against diabetes-induced oxidative stress both in mother and embryos and thus may serve as a therapeutic supplement under diabetic pregnancy.

Mechanism of Nucleoside Uptake in Rat Placenta and Induction of Placental CNT2 in Experimental Diabetes

The purpose of this study was to clarify the transport characteristics of nucleosides in rat placenta and the changes of functional expression of nucleoside transporters in rat placenta with experimental diabetes mellitus. Placental uptake clearances of [(3)H]adenosine and [(3)H]zidovudine from maternal blood was much higher than that of [(14)C]mannitol. Xenopus oocytes injected with rat ENT1 and ENT2 cRNA took up [(3)H]adenosine with K(m) values of 6.1 and 26 µM, respectively. [(3)H]Adenosine transport by rat placental brush-border membrane vesicles (BBMV) was saturable and was inhibited by nitrobenzylthioinosine (NBMPR), a specific ENT inhibitor, in a manner consistent with involvement of both rat ENT1 and ENT2. [(3)H]Didanosine was modestly taken up by placenta, and the inhibitory effect of 100 µM NBMPR on [(3)H]ddI uptake by BBMV suggested a role of ENT2-mediated transport. Expression of ENT1, ENT2, ENT3, CNT2, and CNT3 mRNAs was detected in placenta of control and streptozotocin (STZ)-induced diabetic pregnant rats, and CNT2 (SLC28A2) expression was significantly increased in STZ-induced diabetic rats. Consistently, Na(+)-dependent adenosine uptake by BBMV from STZ-induced diabetic pregnant rats was higher than that from control rats. These results suggest the involvement of placental ENT2 as well as ENT1 in nucleoside uptake from maternal blood, and the induction of CNT2 in experimental diabetes mellitus.

Effects of Quercetin Administration on the Pregnancy Outcome of Diabetic Rats

Objective: Investigate the effects of diabetes and treatment with quercetin on the maternal reproductive performance and impact on foetal growth. Study design: A total of 32 female Wistar rats were distributed into four groups: non-diabetic (G1); non-diabetic treated with quercetin (G2); diabetic (G3) and diabetic treated with quercetin (G4). At day 21 of pregnancy, each rat was anesthetized and humanely killed for laparotomy; was observed reproductive performance, foetal and placental weights and the placental index. Maternal and foetal data were analysed by ANOVA followed by the Tukey test. Foetal weight classification was assessed by Goodman’s test. Results: Diabetes and diabetes treated with quercetin caused placentomegaly an increased placental index and small foetus rates for pregnancy age. Conclusion: Quercetin, administered to pregnant diabetic rats, controlled glucose levels and promoted weight gain compared to untreated diabetic rats, but it did not improve reproductive performance or foetal or placental development.

Abrogation of maternal and fetal oxidative stress in the streptozotocin-induced diabetic rat by dietary supplements of Tinospora cordifolia

ObjectiveDiabetes during pregnancy increases the incidences of congenital anomalies, morbidity, and mortality in the mother and her fetus/newborn. Oxidative stress (OS) has been implicated to be responsible because various antioxidants have been demonstrated to be beneficial in diabetic embryopathy. In this study, we examined the propensity of Tinospora cordifolia (TC) to attenuate embryopathy and OS in pregnant diabetic rats. MethodsPregnant rats were rendered diabetic with streptozotocin (45 mg/kg of body weight, on gestation day 4) and fed a normal or a TC-supplemented (1% or 2%) diet. After monitoring diet intake, body weight gain, and urine output, dams were sacrificed on gestation day 20 and the markers of OS were determined in the maternal liver and the fetal brain and liver. ResultsAlthough streptozotocin induced a significant (40%) increase in embryopathy, the dietary supplements offered significant protection (63%). Interestingly, TC significantly offset the diabetes-associated OS in the maternal liver as evidenced by the lower levels of malondialdehyde (25%) and reactive oxygen species (72%) and the higher levels of glutathione (53%) and total thiols (45%). The protective effects of TC could be observed even in the fetal milieu, with higher levels of antioxidant molecules and enzymes. ConclusionThese data suggest that TC during pregnancy may provide significant protection against diabetes-induced OS and thus serve as an effective therapeutic supplement.

Alternations of phospholipid profile in placenta of streptozotocin‐induced diabetic rat

Phospholipids have important roles in many biological processes, but their role in fetal malformation in pregnancy in diabetes is unclear. Metabolic fingerprinting of placental phospholipids in pregnant streptozotocin-induced type 1 diabetic rats was performed using Fourier transform-ion cyclotron resonance mass spectrometry. Some of the fetuses from the pregnant diabetic rats exhibited ventricular septal defects. Alterations of phospholipid compositions in the diabetic rat placenta were detected. We suggest that these changes in phospholipids in the diabetic placenta might be involved in development of fetal malformation in a type 1 diabetic pregnancy.

Morphological changes in the fast vs slow fiber profiles of the urethras of diabetic pregnant rats

&lt;em&gt;Background&lt;/em&gt;. This study was undertaken to test the hypothesis that diabetes and pregnancy detrimentally affect the normal function of urethral striated muscles in rats, providing a model for additional studies related to urinary incontinence. The aim of this study was to evaluate morphological alterations in the urethral striated muscles of diabetic pregnant rats. &lt;em&gt;Design and methods. &lt;/em&gt;Twenty female Wistar rats were distributed into four experimental groups of five rats as follows: virgin, pregnant, diabetic virgin, and diabetic pregnant. Diabetes was induced using streptozotocin administration (40 mg/kg i.v.). The rats were lethally anesthetized, and the urethra and vagina were extracted as a unit. Cryostat sections (6 µm thick) were cut and stained with hematoxylin-eosin, and immunohistochemical procedures were performed and subjected to morphological and semi quantitative analysis. &lt;em&gt;Results&lt;/em&gt;. The urethral striated muscle from the diabetic pregnant rats presented with the following variations: thinning and atrophy, disorganization and disruption associated with the colocalization of fast and slow fibers and a steady decrease in the proportion of fast &lt;em&gt;vs&lt;/em&gt; slow fibers. &lt;em&gt;Conclusion&lt;/em&gt;. Diabetes and pregnancy impair the urethral striated muscle and alter its fiber type distribution.

Effects of exposure to cigarette smoke prior to pregnancy in diabetic rats.

BackgroundThe purpose of this study was to evaluate the effects of cigarette smoke exposure before pregnancy on diabetic rats and their offspring development.MethodsDiabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group): nondiabetic (ND) and diabetic rats exposed to filtered air (D), diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS) and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP). At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes.ResultsThe association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals.ConclusionDespite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development.

Effect of Matricaria chamomilla L. extract on fetal absorption, placenta structure and liver of diabetic pregnant rats.

Effect of Matricaria chamomilla L. extract on fetal absorption, placenta structure and liver of diabetic pregnant rats.