Placental abruption pathophysiology of diabetes
Your baby might not grow as quickly as expected, and you might have low amniotic fluid or other complications. When to see a doctor Seek emergency care if you have signs or symptoms of placental abruption. Request an Appointment at Mayo Clinic There is a problem with information submitted for this request. From Mayo Clinic to your inbox Sign up for free, and stay up to date on research advancements, health tips and current health topics, like COVID, plus expertise on managing health.
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You may opt-out of email communications at any time by clicking on the unsubscribe link in the e-mail. You'll soon start receiving the latest Mayo Clinic health information you requested in your inbox. Sorry something went wrong with your subscription Please, try again in a couple of minutes Retry Causes The cause of placental abruption is often unknown.
Possible causes include trauma or injury to the abdomen — from an auto accident or fall, for example — or rapid loss of the fluid that surrounds and cushions the baby in the uterus amniotic fluid. What is the most efficient tool? The efficiency of an experimental model is based on the observation of a stable hyperglycemia throughout gestation.
We will then expose genetically predetermined diabetes animal models. The nitrosurea moiety of STZ is responsible for its cellular toxicity, which is probably mediated through a decrease in nicotinamide NAD levels and the production of intracellular free radicals.
In contrast, severely diabetic mothers are insulin deficient, hyperglycemic with low body weight and give birth to microsomic and malformed fetuses. The altered maternal-fetal metabolic fuel relationship resulting from diabetes in pregnancy modulates fetal growth. The increase in fetal glucose and insulin availability with maternal diabetes is strongly associated with the development of fetal macrosomia but severe DM or diabetes of long duration restricts fetal growth.
Merzouk and Soulimane-Mokhtari[ 31 ] verified that mildly hyperglycemic dams have fetuses that are large for gestational age, classified as macrosomic, but this data has been hardly reproduced in other studies[ 32 ]. In , other authors observed an increase of placental weight in their mildly diabetic rats showing a compensatory mechanism to assure the maternal fetal exchanges contribution to fetal development[ 33 ]. The degree of fetal damage and placental dysfunction and the availability and utilization of fetal substrates can lead to the induction of macrosomia or microsomia.
We observed a U-shaped relationship between offspring weight and metabolic changes, like in clinical studies. These models mimic a type 1 diabetic state, despite the lack of immunological and genetic disorders. Nevertheless, some authors have tried to mimic gestational diabetes by varying the doses and the window of injection of STZ in the neonatal period[ 35 , 36 ], before mating[ 37 ] or during pregnancy[ 38 ].
Drawbacks of chemical models: The efficiency of a model is based on the observation of a stable hyperglycemia throughout gestation and depends on multiple parameters such as the dose and mode of injection venous or peritoneal route [ 38 ]. Moreover, the efficiency varies according to the sex, with a lower metabolic sensibility in females[ 39 ]. The authors reported a sexual dimorphism in insulin sensibility with females being less sensitive to insulin than males, leading to a higher susceptibility to the rapid development of a more severe form of diabetes.
In light of these data, it is clear that we have to take into account these variations in experimental model settings. Dietary interventions Exposure to an adverse environment in utero programs the physiology and metabolism of the offspring permanently with long term consequences for health[ 41 ].
This is the basis of the thrifty phenotype hypothesis driven from epidemiological studies showing a strong statistical link between birth weight, further metabolic syndrome and maternal nutrition in a context of type 2 diabetes[ 42 ]. Nutrition is a key environmental factor and it has been shown that inappropriate nutrition in utero has consequences into adulthood[ 43 ].
We speak about nutritional programming as the effect that occurred long after the stressor has been removed. Beta cell development is irreversibly damaged by inadequate nutrition during critical periods of fetal development[ 44 ].
This is a fetus organogenesis adaptation to the fetal-placenta unit environment. Others studies suggest that the post natal period, when catch up growth occurs, may be more important than the in utero period[ 45 ]. The two arguments are now taken into account to suggest that a combination of intrauterine deprivation followed by accelerated post natal growth induce the highest risk of further metabolic disease.
In other words, increased risk of disease arises if there is an imbalance between pre natal and post natal nutritional uptake. This is the basis of two steps nutritional models. We will consider four main nutritional models: high fat, low protein, high carbohydrate and two steps nutritional programming model.
High fat diet model: In humans, consuming a high fat diet model HFD causes an increase in body fat deposition and a decrease in insulin sensibility which leads to insulinoresistance and T2DM. HFD diet is more representative of the eating habits of the current society in both the developing and westernized world. Diets rich in saturated fats before and during pregnancy may result in pathological manifestations in rodents similar to the human condition of GDM. This is explained by alterations in the fatty acid profiles of the membrane of the aorta.
Fatty acid oxidation inhibits both glucose oxidation and its ability to enter cells. Rats fed with HFD develop obesity, hyperinsulinemia and insulin resistance but not frank hyperglycemia and diabetes. Otherwise, by increasing the fat component in the diet, the levels of the other macronutrients would be also affected, leading to nutrient deficiencies. Low protein model: Low protein diet exposure during the first 3 or 6 wk of life in rats have consequences on growth and insulin secretory response[ 49 ].
During pregnancy, these animals are unable to match or adapt to insulin request and become glucose intolerant. Authors concluded that temporary protein energy malnutrition in young rats reduces the ability to increase insulin production to meet the needs of pregnancy. Glucose regulation is perturbed and glucose and other nutrients are transferred to fetuses in increased amounts. The length of diet exposure has an impact on fetus development and physiology.
A diet restricted to the first week of gestation leads to hypoglycemic and low weight fetuses with a high risk of further T2DM[ 50 ]. Carbohydrate model: Infusions of glucose during pregnancy in rats lead to a transient hyperglycemia[ 52 ]. However, significant effects on fetuses need repeated injections of glucose and the window of injection is important with a positive effect restricted to early pregnancy.
This finding matches clinical observations of macrosomia despite a good glycemic control in second trimester. This suggests that metabolic control in early pregnancy is an important determinant for fetal-placental growth throughout gestation. Two steps programming nutritional models: We consider a first step of restrictive diet food restriction, FR30 occurring at the first generation during the 1st period of life and gestation, and a second step of high caloric diet submitted to the offspring after birth and weaning.
Fetuses of this second generation will develop a metabolic syndrome[ 53 ]. Pregnant genetically determined diabetes Pregnant animals with genetically determined type 1 diabetes: The Non Obese Diabetic NOD mice and Bio Breeding BB rats develop spontaneous pre-gestational diabetes and thus represent good candidates for type 1 maternal diabetes models. Stopping insulin treatment induces a loss of maternal weight, ketosis, high rate of fetus resorption, lower fetal weight and higher placental weight[ 54 ].
Therefore, BB rats are a good model for the study of perinatal morbidity, microsomia and malformations. NOD mice develop a mild form of diabetes with macrosomic fetuses and adiposity. It has been shown that maternal hyperglycemia is not the only causative factor of macrosomia, partially explained by a dysregulation of placental glucose transporters and hexokinase protein production unable to protect the fetus from hyperglycemia and hyperinsulinemia[ 55 ].
Pregnant animals with genetically determined type 2-like diabetes: There are models of obesity and diabetes affecting a common pathway, a defect in the leptin receptor db and a defect in the leptin gene ob. The deficiency of leptin has consequences in multiple areas of metabolism, ingestive behavior and reproduction insulin resistance, hyperphagia and infertility.
Most of these experimental models at the homozygous state are infertile. Therefore, mating heterozygotes animals is necessary to inbreeding. After delivery, glycemia reverts to a normal state, making Lepr db mice a good model for GDM investigation. This model induced diabetes and obesity with hyperinsulinemia and hyperlipidemia, and females return to normal weight and glucose tolerance after gestation[ 57 ].
Goto Kakizaki GK is a rodent model of non obese type 2 diabetes that was produced by selective breeding of individuals with mild glucose intolerance from a non diabetic Wistar rat colony. A stable and heritable DM is obtained by selection of a diabetic line isolated by repeated breeding of normal animals[ 58 ]. These rats are not obese and not hyperinsulinemic.
Offspring of GK females is exposed in utero to mild diabetes throughout gestation. Thus, maternal mild hyperglycemia might contribute to endocrine pancreas defects in the first offspring generation. The feto-placental expression of insulin, IGF1, IGF2 and their receptors is regulated in a tissue-specific manner and can be affected by nutritional and endocrine conditions[ 59 ].
Hiden et al[ 60 ] have demonstrated that there is a spatio-temporal change in placental insulin receptor IR expression, suggesting a shift in the regulation of placental insulin effects from mother to fetus. In the first trimester, IR is predominantly expressed on the syncytiotrophoblast facing the maternal circulation, whereas at term, the placental endothelial cells facing the fetal circulation are the main expression site.
They are key modulators of the ligand-receptor interaction. Fetal cord blood data suggest that these binding proteins may be dysregulated by diabetes during pregnancy[ 62 ]. The endocrine interaction between mother, fetus and placenta is exemplified by the effect of maternal and fetal insulin on the placenta.
Maternal insulin affects placental development via receptors expressed on the microvillous membrane of the syncytiotrophoblast[ 21 ]. Fetal insulin affects gene expression in endothelial cells from placental arteries and veins, which will affect placental development. The spatio-temporal change of IR expression in the placenta allows a shift in the control of insulin regulation from the mother to the fetus.
In the first trimester, maternal insulin influences the placenta by interaction with trophoblast IRs. This may in turn affect the mother by secretion of other factors as cytokines and hormones. Later, the fetus takes over control of insulin-dependent placental processes by fetal insulin interacting with placental endothelial cells.
In addition, in the first trimester, IGF1 and IGF2 produced by trophoblasts stimulate various processes that are involved in trophoblast invasion into the maternal uterus such as invasiveness, migration, MMP2 production, proliferation and MT1-MMP expression. Hence, in GDM, transplacental amino acid transport and fetal growth may be promoted by the diabetes-associated increase in maternal concentrations of growth factors.
Changes can also be seen in the fetal circulation. However, the consequences of these changes for the fetus remain unclear. The extensive cross-talk between insulin and leptin signaling cascades may represent a major factor to the diabetes-induced placental changes. In humans, leptin levels correlate with adiposity. This hormone has different functions such as stimulation of angiogenesis, regulation of hematopoiesis and inflammatory response[ 65 ]. The leptin receptor is expressed in the syncytiotrophoblast.
Hauguel-de Mouzon et al[ 65 ] have shown that leptin induces hCG production, enhances mitogenesis, stimulates amino acid uptake and increases the synthesis of extracellular matrix proteins and metalloproteinases. So leptin plays a role in the regulation of placental growth.
However, hyperleptinemia contributes to other placental modifications in the case of diabetes as basement membrane thickening owing to its ability to alter collagen synthesis[ 66 ]. Hiden et al[ 67 ] have proposed a hypothetical model for diabetes-induced alterations in human placenta.
Maternal hyperglycemia induces thickening of the placental basement membrane, hence reducing oxygen transport. Increased levels of placental leptin may even further contribute to the excessive extracellular matrix synthesis. These modifications in the feto-placental compartment are characteristic of GDM, overt diabetes or both[ 67 ].
The nature and extent of these changes depend on the type of diabetes and on the gestational period. For a complex disease syndrome, no animal model can be expected to serve all needs of research. Although each animal model has limitations and strengths, used together in a complementary fashion, they are essential for research on the metabolic syndrome and for rapid progress in understanding the etiology and pathogenesis towards a cure.
Animal models have shown convincingly that diabetes may be transmitted by intrauterine exposure to maternal hyperglycemia. Intrauterine exposure to mild hyperglycemia is associated with normal weight or macrosomic newborns and IGT at adult age, related to a deficient insulin secretion.
In contrast, a newborn offspring of severely hyperglycemic mothers is microsomic and displays, at adult age, a decreased insulin action. In addition, long-term and persistent effects of gestational diabetes on glucose homeostasis in the offspring may be transmitted through generations. These data support the concept of programming of physiological metabolism in offspring by manipulating maternal nutrition. It is known that hyperglycemia is not the only causal factor. Maternal and fetal concentrations of several growth factors, hormones and cytokines are altered in diabetes and may affect the placenta and the fetal development.
It is thus necessary to identify the specific biological effects and the mechanisms underlying them. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus.
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Prenatal ultrasonographic assessment of the ductus arteriosus: a review. Obstet Gynecol. Foetal and placental weights in relation to maternal characteristics in gestational diabetes. Effects of gestational diabetes on fetal oxygen and glucose levels in vivo. Alterations in the activity of placental amino acid transporters in pregnancies complicated by diabetes. Altered activity of the system A amino acid transporter in microvillous membrane vesicles from placentas of macrosomic babies born to diabetic women.
J Clin Invest. Serum-dependent effects of IGF-I and insulin on proliferation and invasion of human first trimester trophoblast cell models. Histochem Cell Biol. Madsen H, Ditzel J. Blood-oxygen transport in first trimester of diabetic pregnancy. Acta Obstet Gynecol Scand.
Transcription factors having impact on vascular endothelial growth factor VEGF gene expression in angiogenesis. Med Sci Monit. Regulation of fibroblast growth factor-2 expression in pulmonary arterial smooth muscle cells involves increased reactive oxygen species generation.
Am J Physiol Cell Physiol. Hyperglycaemia in vitro alters the proliferation and mitochondrial activity of the choriocarcinoma cell lines BeWo, JAR and JEG-3 as models for human first-trimester trophoblast. MT1-MMP expression in first-trimester placental tissue is upregulated in type 1 diabetes as a result of elevated insulin and tumor necrosis factor-alpha levels. Baird JD, Aerts L. Research priorities in diabetic pregnancy today: the role of animal models. Biol Neonate. Impaired insulin secretion after intravenous glucose in neonatal rhesus monkeys that had been chronically hyperinsulinemic in utero.
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