Main DocumentA doctor might order a test of the sugar level in a person's blood if there is a concern that they may have diabetes, or have a sugar level that is either too low or too high. To compare the Lipid peroxidation and Total antioxidant status in women with gestational diabetes mellitus and normal pregnancy in our higher the prevalence of type 2 diabetes in the population 2004) Diabetes mellitus in pregnancy in an African population The problem with this solution is that you will need to snack all day long and that nocturnal hypoglycemia is very difficult to prevent. Cystitis – a lower urinary tract infection that is most common and affects the bladder.
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The Role of Placenta in the Fetal Programming Associated to Gestational DiabetesCarlos Escudero1, Marcelo Gonzalez2, Jesenia Acurio1, Francisco Valenzuela1 and Luis Sobrevia3[1] Vascular Physiology Laboratory, Group of Investigation in Tumor Angiogenesis (GIANT), Department of Basic Sciences, University of Bio-Bio, Chillan, Chile[2] Vascular Physiology Laboratory, Department of Physiology, University of Concepcion, Concepcion, Chile[3] Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynecology, Faculty of Medicine, School of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile1.
As of 2014, an estimated 382 million people worldwide have diabetes according to the International Diabetes Federation. One of the leading researchers of Diabetes Leonor Guariguata estimates that the War on Diabetes while entirely winnable is being lost and that the numbers presented currently are far too conservative.
Presently, the number of people with Type 2 diabetes is expected to double in less than 25 years. Approximately 80% of the people living with diabetes are in low and middle-income countries.
Even scarier is the fact that approximately 316 million people have Impaired Glucose Tolerance  commonly referred to as Prediabetes. Diabetes or as it’s known in medicine, Diabetes Mellitus is a chronic disease that occurs when the pancreas is no longer able to produce insulin, or the bodies inability to utilize the insulin it creates.
Insulin is a hormone created by the pancreas and as such it allows the body to convert glucose from the foods we consume into energy so that our blood cells can utilize it to function properly.
For diabetics, this is a problem as they are unable to produce insulin or use it efficiently which in turn leads to volatility in their glucose levels. People afflicted with Type 1 diabetes, cannot produce insulin, a hormone necessary to convert glucose into energy. Individuals afflicted with Type 2 diabetes, have developed a resistance to the insulin produced within their bodies. This type of diabetes occurs as a result of hormonal changes in a woman’s body during pregnancy.
17% of babies in 2013 were born to women with high blood sugar levels, a sign of gestational diabetes.
The high school dropout rate among diabetics was 6% higher than the dropout rate among their peers. The likelihood that a diabetic student will attend college is 8 to 13% lower and that over the course of a lifetime, a diabetic could lose more than $160,000 in wages. The body naturally tightly regulates blood glucose levels as a part of metabolic homeostasis. The test, which is also called a check of blood sugar, blood glucose, fasting blood sugar, fasting plasma glucose, or fasting blood glucose, indicates how much glucose is present is present in a person's blood.When a person eats carbohydrates, such as pasta, bread or fruit, their body converts the carbohydrates to sugar - also referred to as glucose.
If you still have diabetes after your baby is born it’s likely that you already had diabetes before you became pregnant. Hypogl Caused by too much insulin or oral agents too ly Hyperglycemic Hyperosmo Predominated by hyperosmolarity and hyperglycemia Minimal ketosis Osmotic diuresis HH Occurs more often in older people Type 2 diabetes mellitus No. It covers research about the physiology and pathophysiology of Diabetes mellitus type 2 Diabetic Foot Ulcer Differential Diagnosis California Torrance Classification and external resources Universal blue circle symbol for diabetes.[1] ICD 10 To compensate for low glucose Diabetic Foot Ulcer Differential Diagnosis California Torrance availability as a fuel the body converts fat into ketones for use as an Diabetic Foot Ulcer Differential Diagnosis California Torrance alternative fuel.
WASHINGTON (Reuters) – People who ate a low-fat vegan diet cutting out all meat and dairy lowered their blood sugar more and lost more weight than people on a standard American Diabetes Association diet researchers said on Thursday. Gestational diabetes is usually diagnosed Gestational diabetes happens when your body can’t make enough insulin Clinical trials look at safe and effective new ways to prevent In type 2 diabetes the diabetes risk factors ethnicity headquarters association american address body cells resist the effects of insulin making it difficult for insulin to move sugar out of the blood and into the body cells.
The second commonest type is nephrogenic diabetes insipidus which is caused by the kidneys being insensitive to the anti-diuretic hormone due to drugs or kidney disease. Active Kids Calcium Milk + Vitamin D3 Gummies provide a combination of Vitamin D3 and Calcium which will contribute to normal energy-yielding metabolism normal muscle function normal function of digestive enzymes. Role of feto-placental endothelial function in fetal growth during normal pregnancy and gestational diabetes. In the next 20 years, it is estimated that 1 in  10 people will have Diabetes which would result in approximately 592 million having diabetes by 2035. It disrupts lives, affects family, work and friendships and above all else puts a great deal of strain on the healthcare system.
Too high of a level results in hyperglycaemia which over a long period of time can damage the body through organ and tissue failure.
Most Type 2 diabetics are although a growing number of research has indicated that young people are at severe risk of becoming Type 2 diabetics very early in their life.
It can increase both the mother and child’s risk of getting Type 2 diabetes later on in their respective lives.
Glucose travels through the blood to supply energy to the cells, to include muscle and brain cells, as well as to organs. Diabetic Foot Ulcer Differential Diagnosis California Torrance baring this in mind somebody who shows the symptoms of adult diabetes shouldn’t simply dismiss them as diabetes is a serious and potentially life-threatening disorder but a disorder which nonetheless can be treated extremely effectively.
Most people with type 1 diabetes need to start injecting insulin as soon as they are diagnosed. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.
Finns det ngon Natural Remedies For Diabetic Patients Gestational Abruption Placental koppling mellan Alzheimers sjukdom och Diabetes Mellitus?
Complete information about Diabetes Type II including signs and symptoms; conditions that TYPE 2.
The symptoms of rashes caused by fungus depend on the area of the body which is infected as well as Individual has diabetes.
While there is currently no cure, there are a variety of different things that can be done to help manage gestational diabetes. Estimation of the epidemiological impact of GDM has indicated that at least 1 out of 10 pregnant woman is being affected by GDM worldwide.
Blood sugar levels usually fluctuate depending upon what a person eats and how long it has been since they last ate. Everything you need to know about can diabetes cause hallucinations including the most common causes symptoms and treatments. Department of Biomedical Sciences, Chieti University and San Valentino Vascular Screening Project, Pe, Italy. Natural Remedies For Diabetic Patients Gestational Abruption Placental begitu banyak web yang adatapi cuma web anda yang menurut saya bermanfaatterimakasih. Medicare also covers these tests if 2 or more of diabetes symptoms these apply to you National Diabetes Education Program. These transport mechanisms are in a perfect equilibrium between demand and consumption, and they are highly dependent on the appropriated endothelial function in the placental vascular bed.
In addition, GDM causes not only short-term complication in both mother and fetus, but also is associated with elevated risk for long-term complication such as cardiovascular disease, obesity and diabetes. Many people think of diabetes as the Diabetes gestacional: Es aquella que se diagnostica durante el embarazo. Nhs Diabetes Blood Sugar I’m here to point you to presume I have a loathing in relation to blood glucose meter. NHS Choices - its 'understanding diabetes' pages offer comprehensive information on symptoms, diagnosis and treatment. In the images is presented only HUVEC that were seeded at 30 x 103 and hPMEC that were seeded at 10 x 103. Preliminary results in our laboratory suggest that gestational diabetes mellitus (GDM) is associated with elevation of adenosine extracellular levels and high activation and expression of A2A adenosine receptor characterized by high (?) eNOS activation, NO formation and Y-nitration whose are associated to enhancement of cell proliferation and migration and finally it would be occasioned elevated placental angiogenesis characteristic of this disease.7. Urine again and again and have more volume and sweetness of urine voiding the ants take place . Those cells were maintained in culture under standard conditions (5% CO2, 37oC) during 0, 1, 2, 3 and 4 hours and cells were photographed. Part of this adaptive response, might also include the elevation in the placental consumption of glucose and enhancement of the feto-placental blood flow, especially in fetus large-for-gestational age (LGA). What this means is a person will not be able to drink or eat for 8-10 hours before the test, or the doctor may order the test for a random time or right after the person eats.
BioHub FAQ; Support DRI centers and a data coordinating center established in 2004 to conduct studies of islet transplantation in patients with type 1 diabetes. With a glucose monitor at home people could keep track of their glucose levels 8 2014 (HealthDay News) Technology can ease some of the burden of managing diabetes possibly getting blood sugar levels within safe ranges more People with week immune system like those having diabetes have a higher risk of urinary tract infections. Both, vasomotor and angiogenic properties are modulating the fetoplacental blood flow continually by a cross talking between placenta and fetus. As indicated in the pictures, hPMEC exhibit a more rapid response for tube formation under our culture condition and require lesser quantity of cells than HUVEC, suggesting a differential physiological role of these cells in the fetal circulation. On the other hand, due to lack of innervation in the placenta, the vascular tone is controlled by the regulation of the synthesis and release of vasoactive substances from the endothelium like vasoactive molecules, nitric oxide, adenosine, prostaglandin, among others.
If a woman is pregnant, her doctor might order a, 'glucose-tolerance test,' which involves drinking glucose solution and having blood drawn a specified amount of time later. On the other hand, there is an increase in the glucose level in the maternal circulation in gestational diabetes mellitus (GDM), which is transported to the feto-placental circulation generating and stated of hyperglycemia, hyperinsulinemia and insulin resistance. In turn this high glucose uptake may generate elevated oxygen consumption due to high metabolism.
In this regard, several studies have shown that placenta from GDM is characterized by hypervascularization and elevation in the pro-angiogenic signals including the secretion and activity of the vascular endothelial growth factor (VEGF).
This elevation in the glucose metabolism in the placenta would generate an endothelial dysfunction characterized by elevation in RNS, ROS, prostaglandin and purine concentration in the feto-placental circulation, which consequently affects the tone regulation in the placenta.
In addition, hyperglycemia also generates a status of oxidative stress, where free radicals derived from oxygen (ROS) induces changes in the endothelial cell membranes producing an elevation in the cell permeability. With the exceptions of insulin, exenatide, liraglutide and pramlintide, all are administered orally and are thus also called oral hypoglycemic agents or oral antihyperglycemic agents.
Moreover, relative hypoxic condition in GDM, may trigger an pro-angiogenic response generating a condition of hypervascularization in the placenta and therefore creating a vicious circle.
A doctor who is concerned might order additional testing at 1,2 and 3 hours after a person drinks glucose. In this chapter, we will review the available literature focus on the role of feto-placental endothelial dysfunction as the possible main factor in the generation of short-term complication during GDM and speculate how it may program the response of the sibling exposed to GDM.2. Finally, this high input of nutrients and elevated circulation will be responsible for macrosomia in GDM. Gestational diabetes: Definition and epidemiologyPregnancy is a physiological state where occurs a series of complex anatomical and functional adaptation in the mother to facilitate the development of fetus. For instance, during the normal pregnancy a “physiological” insulin resistance is necessary to provide glucose to the growing fetus [1].
However, this normal adaptation is no longer occurring in some conditions and generates a clearly pathological state of insulin resistance, which is called Gestational Diabetes Mellitus (GDM). Additional causes of hypoglycemia include hypothyroidism, hypopituitarism and having taken certain kinds of medications.

Therefore, GDM has been defined as any degree of glucose intolerance with onset or first recognition during pregnancy [2]. This discrepancy has been extensively discussed in the literature but the general agreement is that adverse perinatal outcomes occur in lesser degrees of hyperglycemia than the recommended as diagnostic criteria by the WHO [4].Prevalence of diabetes for all ages is increasing worldwide, including women in fertile age.
A1C test levels of greater than 7% reveal poor diabetes management and the need for changes in the future.
Therefore, it is not surprising that diabetes diagnosis before or during gestation has been defined as a public health problem [5].
Epidemiologically speaking, it has been estimated that near to 90% of the diagnosis of diabetes in pregnancy is actually GDM [5].
Usually, high blood sugar levels have to do with a poor diet, but even more often they have to do with a person's lack of exercise and physical activity.A number of medical studies have shown a dramatic relationship between elevated blood sugar levels and insulin resistance in people who are not very active on a daily or regular basis. Many of the same studies have also shown that the most efficient way of improving insulin resistance is to increase the amount of physical activity. Thus, taken into account the origin of the population, it has been described that women from Asian, African American, and Hispanic background exhibit twice the risk for being diagnosed of GDM compared to those of non-Hispanic White origin, a phenomenon observed also in women in the lowest socio-economical quartiles compared to women in the highest quartiles [8,9].
Doing so helps a person to achieve weight loss, increase blood flow and circulation, as well as lower blood sugar levels.Deciding to begin exercising and become active also involves beginning to eat better.
The underling mechanisms responsible for GDM are under investigation; however, likewise to other causes of type 2 diabetes, GDM is characterized by a dysfunction in the pancreatic ? cell, which does not produce enough insulin to meet the increased requirements of late pregnancy.
Changing eating habits alone will help, yet doing both together will supercharge a person's efforts. Try to find a cookbook filled with quality foods and meal plans that are ideal for people with diabetes, people with pre-diabetes, as well as those with high blood sugar levels who might be insulin resistant.
In addition, it has been described that the large majority of the insulin secretory defects present in the third trimester of gestation, are actually manifesting before and soon after pregnancy [10,11]. In this way, considering that a) obesity, is a condition of insulin resistance and a common risk factor to GDM, and b) insulin secretion during pregnancy increases according to gestational age in women with and without GDM [10]; it has been reinforced the concept that chronic deficiency rather than gestational-acquired deficiency of insulin secretion is the underling cause for GDM.
Consequently, these evidences have broken the traditional vision of GDM pathogenesis, where the imbalance in glucose level at the third trimester of gestation has been consider exclusively as a defect in the “physiological” insulin resistance present in pregnant women.
With regard to insulin, it is well known that it reduces the elevated level of blood glucose; however, insulin is also regulating the metabolism of amino acids and lipids.
Indeed, selective damage of ?-cell in animal models generates a severe lipid defects that induce animal death [12,13]. This idea reinforces the general agreement of hyperglycemia is not the unique feature that may be taken into account during GDM management. In addition, it has been reported that in general, hyperglycemia is resolved after birth; however, there are epidemiological evidences showing that GDM constitutes a risk factor for development of diabetes mellitus type 2 (DMT2), as well as it constitutes a risk factor for hypertension in both mother and offspring.
Thus, it has been estimated that about 10% of women with GDM have diabetes mellitus soon after delivery; whereas the rest will develop diabetes mellitus at rates of 20-60% within 5-10 years after the manifestation of GDM in the absence of specific interventions to reduce their risk [10]. Therefore these evidences have suggested that metabolic defects in GDM, characterized by hyperglycemia, and fundamentally, insulin deficiency (relative in GDM) are maintained after birth being a risk factor for metabolic and cardiovascular diseases in the mother and her sibling. Thus, considering data on the difference in the birth weight between the lowest and the highest glucose categories was about 300g. Therefore, this study suggests that maternal hyperglycemia, even in the “normal” range according with the WHO criteria, is related to clinically important perinatal disorders. When the authors excluded the HAPO study from their meta-analysis, the relative risks for the analyzed perinatal outcomes were minimally altered.
This association between GDM and macrosomia is particularly important for our discussion, since it has been described that fetal growth defects are associated with long-term complication, including obesity and diabetes [15,16]. Nevertheless, another highlight of this meta-analysis is that reduction in the criteria for “hyperglycemia” recommended by the WHO, should be considered for the next generation.Although discrepancies in cut off value of glucose level for diagnosis of GDM, most of the alterations observed in GDM have been related with “hyperglycemia”.
For instance, it has been shown that intraperitoneal injections of high glucose in early pregnancy were associated with a modest but significantly increased placental weight and fetal weight [17].
Therefore, authors suggest that increased fetal growth may be explained by a large placenta and delivery of more nutrients to be transferred to the fetus.
Since macrosomia is also present in “normo-glycemic” pregnant women, it has been suggested that other factors rather than high glucose by itself may take part in the pathophysiology of maternal and fetal-neonatal complication present in GDM [18].
In this way, other clinical components in GDM, included metabolic alteration such as insulin resistance, as well as high levels of cholesterol, triglycerides, adenosine, nitric oxide, and several other factors may disrupt normal function of maternal, placental and fetal tissues. Specifically, it is well accepted that hyperglycemia in the fetus exposed to GDM, generates a compensatory elevation of insulin; which in turn, is not only affecting glucose level, but also is acting as a growth factor.
In addition, insulin is also regulating the transport of other nutrients such as amino acids or other regulatory elements such as adenosine [19,20,21]. In particular, it has been described that insulin increases the L-arginine uptake in human umbilical vein endothelial cells (HUVEC), a phenomenon associated with generation of vein relaxation and increasing Sp1-activated SLC7A1 (for human cationic amino acid transport type 1, hCAT-1) expression [22]. In addition, it has been described that insulin increases the activity of neutral amino acid through the system A [23].
On the other hand, insulin recovers the reduced adenosine transport mediated by the Equilibrative Nucleside Transport type 1 (ENT-1) in HUVEC, an effect that was associated with increased relaxation of the umbilical vein [24]. In the next section, it will be reviewed some of these evidences and the mechanisms linked with fetal programming in GDM.4. Programming and GDMProgramming is defined as "the phenomenon whereby a stimulus occurring during a critical window of development, namely the prenatal and early postnatal periods, which can cause lifelong changes in the structure and function of the body” [25].
In this regard, the concept that the intrauterine environment might affect health later life became evident with the surprising observation that low birth weight was associated with increased cardiovascular disease 40 years later [15,16,26]. Numerous epidemiological studies extended these observations to suggest a role for the intrauterine environment as a leading cause of schizophrenia, depression, cardiovascular diseases, stroke, diabetes, cancer, pulmonary hypertension, osteoporosis, polycystic ovarian syndrome, among others in adult life [27,28,29,30].
These observational relationships are supported by animal experiments, which fetal growth manipulation by changing maternal nutrition or reducing blood flow to the placenta resulted in obesity, increased blood pressure and other cardiovascular abnormalities in the offspring later life [31]. In addition, a clear association between maternal diseases (including GDM) and future implication in health in the offspring has been affected by several confounding variables such as genetic factors (a particular phenotype may be genetically transmitted to the offspring), paternal implication (the father genotype may affect the phenotype), gender (hormonal differences may induce a particular gender-linked phenotype), diagnosis criteria used for maternal disease (in the particular case of GDM, the level of glycaemia), retrospective evidences (most of the epidemiological analysis coming from retrospective rather than prospective studies), among others.
Despite those confounding factors, most of the available data in the case of GDM supports a predominant role for intrauterine exposition to hyperglycemia as one of the underling mechanisms for future chronic disease in the offspring exposed to this disease [25]. Among the evidences that support this assumption, it has been described that children born after a diabetic pregnancy in Indian Pima women exhibited a high (6-fold) prevalence of type 2 diabetes than those who were born from a non-diabetic pregnancy. Interestingly, this high prevalence persists after a multivariable analysis, taken into account paternal diabetes, age of onset of parental diabetes in father and mother and obesity in the offspring [32]. Besides, another study showed that the risk of diabetes was significantly higher (? 4 fold) in siblings born after GDM than those who were born before the mother has been diagnosed with diabetes [33]. Offspring “exposed” to GDM shows a high risk for developing obesity, impaired glucose tolerance, type 2 diabetes, malignant neoplasm and hypertension in adulthood [34,35,36,37,38,39]. For instance, initially, it has been reported that offspring (10-16 years) “exposed” to maternal diabetes showed a higher prevalence (6-fold) of impaired glucose tolerance and body mass index than controls non-exposed [40].
Furthermore, this finding was confirmed in another study including children (1-9 years) who their mothers presented pregestational insulin-dependent diabetes (IDDM) or GDM [41]. Following to this study, prospective data from the Framingham Offspring Study [42], which included a large sample (2.527 subjects), found that offspring (26-82 years) of women with diabetes showed a high risk (?3-fold) to impaired glucose tolerance and type 2 diabetes compared to individuals without parental diabetes. This risk was almost three times higher in children belong to diabetic mothers <50 years. Moreover, another study also confirms these findings, where offspring “exposed” to GDM exhibited ? 7 folds increase in the prevalence of type 2 diabetes or impaired glucose tolerance compared to offspring from non-diabetic pregnancy [39].
Interestingly, this risk was even higher than offspring of women with type 1 diabetes who presented ? 4 fold risk for being diabetic [39], reinforcing the idea that maternal intrauterine environment generates a particular phenotype which is not explained only by heritage.
Nevertheless, Clausen et al (2009) have reported a high risk (? 2 fold) for developing overweight or metabolic syndrome in offspring of women with GDM or type 1 diabetes compared to offspring from non-diabetic pregnancies.
It has been also reported that the higher hyperglycemia in the mother [36] or the weight for gestational age in children exposed to GDM [43], the higher risk for metabolic syndrome in the offspring in future life. Moreover, GDM is also associated with high risk for cardiovascular diseases in the offspring. Thus, in a large cohort study, it has been reported that children exposed to GDM had higher systolic blood pressure (?3 mm Hg) than non-exposed children [44]. Interestingly, a significantly higher risk for those groups of diseases were also observed in children whose mother had type 1 diabetes or pre-gestational type 2 diabetes. Therefore, a hyperglycemic intrauterine environment seems to be part of the pathogenesis of chronic metabolic and cardiovascular disease in the offspring of GDM [36,37,39].
The mechanisms linked with fetal programming during GDM have been associated with hyperglycemia, through the hypothesis of fuel-mediated toxicity (Freinkel’s hypothesis) [46], which indicates that fetus experiences a “tissue culture” environment, in such circumstances, where high availability of nutrients may induce a “fuel-mediated teratogenicity”. Particularly, we will focus on the alterations observed in the placental vasculature, early in life, that may support the association between elevated risk for cardiovascular disease during adulthood and GDM. Since placental circulatory system form a continuous network with the fetal circulation, it is feasible to propose that changes in the function and regulation of all these vessels early after birth may give clues of the abnormalities that will occur later in life.5. The placenta prevents the passage of macromolecules over 700 Daltons, whereas the smallest particles can cross (for instance melatonin, catecholamines and other hormones) [49,50]; therefore, this tissue exhibits a selective permeability that is known as the placental barrier.
In the formation of human placenta, the maternal vessels are invaded by trophoblastic cells, which in turn are in direct contact with maternal blood. In the maternal side, a laminar degenerative process in the junctional zone forms the maternal layer or uterine surface, which in general are formed by maternal vessels where the endothelium has been replaced by placental cells (invasive cytothrophoblast), remnants of endometrial glands and connective tissue.
Moreover, grooves is shown in this structure, which subdivide the surface of placenta in about 10-40 elevated areas similar to lobules named maternal cotyledons, which are in perfect correlation with fetal cotyledon [51].
The fetal component, cotyledon, is formed by several villous trees (1-3 villous trees per fetal cotyledon), which in fact are formed by chorionic villus. Cytotrophoblast and differentiated syncytiotrophoblast are derived from trophoblastic cells. The syncytiotrophoblast is a multinucleated and continuous layer of epithelial cells, which is formed by the fusion of cytotrophoblasts. In the other hand, syncytiotrophoblast is covering the villous trees and it is in direct contact with maternal blood, therefore, it is the area where direct exchange of oxygen, nutrient and removal of waste products occurs [53].
Moreover, syncytiotrophoblast have an endocrine function characterized by production of human chorionic gonadotrophin (hCG) regulated by progesterone [50]. Besides, those cells also secrete a variant of growth hormone (GH), human placental lactogen (hPL), insulin-like growth factor I (IGF-I) and endothelial growth factor [50,53]. On the other hand, cytotrophoblasts (or Langhans?cells) are continually differentiating into syncytiotrophoblast. There is a trophoblastic basement membrane supporting these two layers, cytotrophoblast and syncythiotrophoblast. This membrane forms the physical separation of those layers with the stromal core villi, a structure formed by connective tissue where the fetal vessels are immersed. In the placenta, the blood vessels constitute the largest component among the structures creating the cotyledons.
In fact, placental vessels constitute a continuous circulatory system with the fetal cardiovascular system.
In the placenta, the veins are conducting oxygenated blood toward the fetus, whereas the arteries contain deoxygenated blood toward the placenta.
Anatomically, from the umbilical cord to the deep in the placental cotyledons, the umbilical arteries and veins branch themselves to form chorionic arteries and vein, respectively, over fetal surface of the term placenta, and those branches subdivide themselves before entering into the villi.
Likewise other vascular beds, in the placenta the veins are more elastic, exhibit high capacity and a miniscule layer of both smooth muscle cells and adventitia compared to arteries; which in turn are vessels that offer a high resistance. These characteristics, especially those observed in the umbilical cord, have been used for functional non invasive studies, like Doppler, in order to analyze the status of the feto-placental circulation.
Finally, and similar to any other tissue, the placenta blood vessels are lined by the endothelium.

The endothelial cells are supported by a basal membrane and pericytes, both of them involved in vessel permeability and integrity, and importantly in the endothelium differentiation [56].In GDM, it has been reported macroscopical and histological alterations in the term placenta.
On the other hand, regarding studies, in syncytiotrophoblast from diabetes during pregnancy, have shown functional alteration in this cell type.
Thus, it has been described an increase in the number of cytotrophoblast identified by number of nuclei [60], high fibrin deposit over syncytiotrophoblast and hyperplasia of cytotrophoblast [59,61,62], whose in turn may be related with the enhancement of the thickness of syncytial basement membranes in GDM compared to normal pregnancy [63]. Moreover, using functional studies of syncytiotrophoblast microvillous membrane vesicles, Jansson and collages [64] showed non-changes in the glucose transport in samples from GDM. Contrarily, other reports showed reduced glucose uptake and glucose utilization [65], as well as low expression of glucose transporter type 1 (GLUT1) and 3 (GLUT 3) in placentas from GDM compared with non-diabetic controls [66]. Other alterations in the throphoblastic cells from GDM were low expression of serotonin transporter (SERT) and receptors (5-HT2A) [67], as well as high activity of amino acid transporter system A [68]. Nevertheless, it has been reported a high expression of inducible nitric oxide synthase (iNOS) in the whole placenta but mainly in the trophoblastic cells using immunohistochemistry in GDM [69], a phenomena that may be correlated with high nitric oxide synthesis [24] and nitrative stress [70] observed in placentas from GDM. In addition, it has been reported high level of degenerative lesions such as fibrinoid necrosis and vascular lesions like chorangiosis, as well as elevated signs of villous immaturity and presence of nucleated fetal erithrocytes in placentas from GDM compared to normal pregnancy [58].
Thus, it has been reported in GDM that the elevation of plasma glucose in the umbilical vein is associated with reduced oxygen saturation and oxygen content, as well as a significant increase of lactate concentration compared with normal pregnancy [59]. Interestingly, these changes were not observed in the umbilical artery, suggesting high placental oxygen consumption in GDM, which may generate a compensatory response in the placenta itself.
Therefore, placental alteration in GDM includes changes in the transport of nutrients (such as amino acid), enhanced blood formation and glucose consumption that may generate a “relative hypoxic” status.
Unfortunately, all this findings are described in term placenta; therefore, non-invasive test such as Doppler will offer more clinically relevant information regarding fetal status and feto-placental circulation before delivery. Placental blood flow and GDM One of the non-invasive techniques used widely to estimate the blood flow in the feto-placental circulation is Ultrasound and Doppler. Moreover, the absence of end-diastolic blood flow before 36 weeks gestation is utilized clinically as indicator of fetal distress such hypoxia and acidosis [77] and this indicator is also associated to growth restriction [78].
Wharton’s jelly area is surrounding the two arteries and the vein in the umbilical cord, and this jelly has a protective role for preventing interruption of flow by compression or twisting caused by fetal movement [79]. Wharton’s jelly area can be determined by subtraction of umbilical cord area and total vessels area (arteries and vein), and interestingly it is significant correlated with gestational age and fetal anthropometric parameters [79,80], and also it has been described that alterations in this parameter are associated to hypertensive disorders, fetal distress, gestational diabetes and fetal growth restriction [80]. Doppler studies in umbilical vein from GDM have shown no changes neither in the pulsatile index value in the umbilical artery nor in the mean total umbilical venous flow in fetus exposed to GDM compared to normal pregnancy [81].
Interestingly, large for gestational-age fetus showed an increase in the total umbilical venous flow, suggesting that high placental flow toward the fetus may be associated with macrosomia. Moreover in macrosomic fetus without diabetes, it has shown an increase in the umbilical vein blood flow associated with high systolic velocity in the splenic, superior mesenteric, cerebral and umbilical arteries [82], suggesting an increased fetal perfusion especially in the liver.
The underling mechanisms for this redistribution in the blood flow are unclear, but considering that GDM increases the synthesis of nitric oxide in human umbilical vein endothelial cells [83], it is feasible to speculate that a overall vasodilatation in the pre-hepatic and hepatic circulation would be taken part in this process. Taken these evidences into account, it is feasible that elevated feto-placental blood flow and hyperglycemia would be responsible for macrosomia in GDM. These mechanisms include; maintenance of physiological barrier, regulation of vascular tone and angiogenesis. Importantly, feto-placental endothelium forms an uninterrupted tissue that will be extended until fetal circulation, where it is exposed to the same metabolic and hormonal medium than endothelium of the fetus itself [84].
Moreover, since the lack of innervation of the placenta, the regulation of vascular tone is mainly dependent on endothelial cells-mediated synthesis and release of several vasoactive substances including, nitric oxide (NO), prostacyclin, thromboxane, endothelial derived hyperpolarizing factor (EDHF), adenosine, mono or di or tri monophosphate of adenosine (AMP, ADP, ATP), among others [85,86,87]. These characteristics are summarized in the Figure 1, where it also described some functional alterations observed in GDM.
On the other hand, there are emerging evidences showing that endothelial cells are able to dedifferentiate into mesenchymal cells, via a process called endothelial-to-mesenchymal transition (EndMT) [88,89], which in fact is related with the capacity of the endothelium to migrate away from the vessel-lining and colonize other tissues where dedifferentiation may occur in order to recover the particular capacity required by the invaded tissue.
Both, dedifferentiation and vessel formation are mechanisms controlled by extracellular signals that are sensed by membrane receptors in the endothelium. Therefore, it is not surprising that endothelium exhibits a specialized function according with its cell localization and mainly according with the extracellular medium where they are seeded [91,92,93]. Figure 1.Role of feto-placental endothelial function in fetal growth during normal pregnancy and gestational diabetes.
Finally, this high input of nutrients and elevated circulation will be responsible for macrosomia in GDM.Human placenta is an unique source of endothelial cells for studying functional differences considering vessel distribution. Thus, it has been estimated that >70% of the placental tissue is constituted by blood vessels and length of fetal capillaries would be covering an area of 223 miles [91].
In addition, since autonomic control of the vascular resistance will not be part of the mechanisms for controlling blood distribution, endothelial cells are responsible for supplying this lack. Moreover, in human placenta, several studies have been shown that endothelium exhibits morphological and functional differences according to the vascular bed where they are coming from [84,87,91,92].
For instance and similarly to the pulmonary circulation in the adult, the feto-placental endothelium has a particular distribution.
The veins transport oxygen and nutrients whereas the arteries contain de-oxygenated blood coming from the fetus.
In terms of endothelial-derived vasomotor response, it has been described that acute hypoxia in the placental microvessels generates constriction [95], whereas this challenge generates augmentation of the umbilical blood flow [96]; this phenomenon is attributed to blood redistribution such occurs in the pulmonary circulation. In addition, HUVEC (i.e, macrovascular endothelium) showed a reduced synthesis of angiotensin II, thromboxane B2, 6-keto-prostaglandin, and endothelin 1,2 compared to placental microvascular endothelial cells (hPMEC) [91]. Thus, placental microvascular placental cells exposed to VEGF or placental growth factor (PlGF) showed a high mitogen response compared to HUVEC [91], a phenomena associated with high expression of VEGF receptor 1 (VEGFR-1) and 2 (VEGFR-2) [98] in this cell type. In addition, using feto-placental tissue it has been described that several genes related with angiogenic response are preferentially expressed in microvascular than macrovascular endothelium [86,87,91,92]. As indicated in the pictures, hPMEC exhibit a more rapid response for tube formation under our culture condition and require lesser quantity of cells than HUVEC, suggesting a differential physiological role of these cells in the fetal circulation.Several studies have reported dysfunction of feto-placental endothelium during GDM [18,74,75,84,86,91,93,99].
For instances, it has been described that L-arginine transport- mainly via the cationic aminoacid transport type 1 (CAT-1) - is increased in HUVEC from GDM [87,100,101,102].
Besides this alteration, it has been described high expression and activity of endothelial nitric oxide synthase (eNOS) [24,103] as well as iNOS [69] in both umbilical and placental endothelium from GDM.
This enhancement would produce a high synthesis and release of NO [20,24], which in turn has been related with a nitrative status in the placenta and umbilical cord from this disease [104,105].
In addition, NO reduces the expression of adenosine transport via hENT-1 [83] and may generate augmentation in the extracellular level of adenosine in umbilical blood [106].
In turn, adenosine activates adenosine receptors (AR) spreading the vascular effects of NO in the feto-placental circulation in both vascular tone regulation [87,100,102] and promoting angiogenesis (see below).
Therefore, it is feasible to speculate that the elevation in NO synthesis during GDM may explain the augmented umbilical flow observed in macrosomic fetuses [82].
GD and oxidative stress in the placentaAs detailed above, GDM has been associated with impaired placental development characterized by high placental weights and low ratios between fetal and placental weights [107].
Remarkably, one of the cellular mechanisms associated with the etiology of these changes is the oxidative stress, which is related with an imbalance between the synthesis of reactive oxygen and nitrogen species (ROS and RNS, respectively) and the activity of antioxidant enzymes. The most relevant free radicals are superoxide (O2•-) in the ROS group; and nitric oxide (NO) and peroxinitrite (ONOO-) in the RNS group. In addition, considering the diffusion distance, NO can diffuse from endothelial cells to smooth muscle cells, whereas O2•- and ONOO- would have actions within the cells where they were synthesized [70]. In fact, it has been described that the elevation in the normal metabolic rate of feto-placental tissues increases the oxidative stress in the placental [109].
Moreover, in placental tissue from early pregnancy has been determined a higher activity of NADPH oxidase; therefore, the synthesis of O2•- is more marked at the end of the first trimester than the activity in term placental tissue [110].
On the other hand, studies using samples obtained from patients with GDM showed that there is an increased activity of xanthine oxidase (XO) and a decreased activity of catalase in maternal plasma, umbilical cord plasma and placental tissue [111]. These findings showed that there is an impairment of antioxidant defenses in the placenta and blood from mother and newborn, which might be related with the high mortality and morbidity in both mother and newborn observed during GDM pregnancies. In addition, placental tissues from GDM exhibited a decreased response to oxidative stress induced by hypoxanthine plus XO, as was reflected by a reduced levels of catalase and glutathione peroxidase (GPx) after exposition to the pro-oxidative challenge, suggesting that placental tissues from GDM would be exposed to damage in an oxidative environment [112].
The hallmark of diabetes is hyperglycemia whose condition has been associated with increases of synthesis of ROS and RNS in tissues and cell cultures from umbilical cord and placenta. There is an increase of ROS levels in HUVEC exposed to high extracellular concentration of D-glucose mediated by activity of NADPH oxidase in a mechanism that involved a decrease of NO bioavailability and increases of vascular reactivity in umbilical veins [21,113]. In HUVEC, it has been described that the higher increase in the NADPH oxidase-mediated ROS induced by high concentration of D-glucose, the higher NO synthesis mediated by eNOS [21,113]. Considering the reaction rate between O2•- and NO, it is highly probable that the hyperglycemic condition induces the synthesis of ONOO-; therefore, it contributes to the development of endothelial dysfunction in umbilical cord and placenta. Long-term incubation (7-14 days) of HUVEC with high concentration of high D-glucose increases the expression of regulatory subunits of NADPH oxidase p67phox and p47phox [114], whereas 24 hours incubation of the same cell type with high D-glucose increases the expression of the catalytic subunits NOX2 and NOX4 [113].
Thus, an increased expression and activity of NADPH oxidase would be a hallmark of HUVEC exposed to hyperglycemic, suggesting that the same phenomenon would be present in GDM.On the other hand, recently data has been shown that in trophoblastic cells ACH-3P, incubated at 21 % oxygen and under normoglycemic condition, increases ROS levels after 3 days.
Interestingly, ACH-3P cells treated (3 days) with high extracellular concentration of D-glucose increases the ROS levels only in cells exposed to lower percentage of oxygen (2.5 %). Therefore, this study is showing that ROS production in normoglycemia is oxygen-dependent but oxygen-independent in hyperglycemia.
In summary, there is an imbalance in the control of redox cellular status in pathological conditions related with increases blood concentrations of molecules that induce oxidative stress, like GDM and hyperglycemia, probably due to a higher expression of oxidant enzymes like NADPH oxidase, XO and deregulation of metabolic pathways of NO.Placental angiogenesis and GDM Angiogenesis is a general term that involves the physiological process leading to growth of new blood vessels from a pre-formed one. This is a vital process involved in embryological growth, tissue development, would healing of damaged tissues and in the context of this chapter is a crucial process for placental development and fetal growth during normal and GDM.
In this regard, as it has been remarked before, macrosomia, present in GDM, has been associated to increased nutrient delivery toward the fetus, a phenomenon that may be related with increased blood flow due to vasodilatation of placental vessels [100].
Thus, placentas from GDM exhibits elevated number of redundant capillary connections per villi, compared to normal pregnancy, suggesting a more intense capillary branching [120]. Moreover, there are increased placental capillary length, branching and surface area that have been reported in women with type 1 [121], pre-gestational and gestational diabetes [18,74], as well as elevated number of terminal villi and capillaries in women with hyperglycemia [73].
In addition, it has been reported that glycemic control was significant correlated with capillary surface area and capillary volume in women with pre-gestational diabetes [117]. Moreover, it is well known that diabetes is associated with increased angiogenic response in some specific tissues such as eye, where hyperglycemia can lead to retinopathy [122]. Nevertheless, it has been shown that GDM is associated to reduction in the circulating endothelial progenitor cells (EPC), in mother and fetus [123,124] a phenomenon that was linking with reduced capacity for recovering endothelial dysfunction in GDM.Associated mechanism behind increased placental angiogenesis in GDM may be related to the pro-angiogenic effect of hyperglycemia [125], which in turn triggers an enhancement in the placental synthesis and release of VEGF, as well as the expression of VEGF receptors (VEGFR) and nitric oxide production [18]. Thus, it has been shown that the placentas from women with hyperglycemia exhibited high levels of VEGF and VEGF receptor 2 (VEGFR-2) but reduced expression of VEGF receptor 1 (VEGFR-1) [73]. Furthermore, it has been reported elevated placental levels of VEGFR-1 mainly in vascular and throphoblastic cells in women with GDM [73,126]. Also, alteration in VEGF-VEGFRs expression has been described in women with type 1 diabetes [18,61,75,127].
Thus, the increased secretion and activity of VEGF may explain hypervascularization observed in placentas from DGM [58,71] On the other hand, increased placental angiogenic response may also be related with hyperinsulinemia present in GDM. In this regard, it has been described that insulin activates at least two types of insulin receptors (IR), type A (IR-A, associated with a mitogenic phenotype) and type B (IR-B, associated with a metabolic phenotype), which are elevated in both HUVEC [24] and hPMEC [106], respectively. Another potential pathway, involved in the increase of placental angiogenesis during GDM, may be the ALANO pathway described before [100].
In this regard, we have previously proposed that a dysfunction in this pathway is taken part in the physiopathology of reduced placental angiogenesis in pre-eclampsia [129].

Blood glucose test lab report discussion
Fasting blood glucose level of 109
Blood glucose testing alternative sites


  1. 30.11.2015 at 16:11:16

    Molecules become glycosylated, which impairs the.

    Author: Hellaback_Girl
  2. 30.11.2015 at 18:19:17

    Re-examine the meal plan or insulin your health care team.

    Author: VASYAK