Diabetes is a disease where your body cannot control its blood sugar levels properly – either because your body doesn’t make enough (or any) insulin, or because your cells have become resistant to insulin. Insulin is produced in the pancreas, it is important because it helps your body process sugars.
Diabetes can affect the body in many other ways, including eye disease, foot ulceration, kidney failure, amputation and a higher risk of heart disease.
Keeping your blood sugar at a safe level means you’re less likely to experience other health problems.
If diabetes is diagnosed and managed effectively, you can still live a long and happy life as long as you stay in control. There are also many people in Fiji living with diabetes who may not even know it because they don’t have the symptoms, it is important to get your blood sugar tested regularly to avoid Diabetes related complications further down the track. The 2002 STEPS survey identified that out of the 16% diabetics, 50% of them were previously unrecognised which is an alarmingly high number.
Given the fact that 30% of Fijians have Diabetes, you have a 1 in 3 chance of having or developing diabetes.
Early detection and treatment of diabetes can decrease the risk of developing the complications of diabetes. The best way to check if you have diabetes or are at risk is to visit your local health centre. This chart shows the different levels of blood glucose, what are safe levels and what are dangerous levels depending on when you last ate. Even if you have no symptoms at all, it is important to get tested as you may still have diabetes.
You can prevent or delay the onset of Type 2 diabetes through adopting a healthy lifestyle.
By changing your diet, increasing your level of physical activity and maintaining a healthy weight, you can stay healthier, live longer and reduce your risk of Type 2 Diabetes.
Type 2 diabetes occurs when your cells have become insulin resistant or your body doesn’t produce enough insulin to keep you healthy. An Oral Glucose Tolerance Test (OGTT) may be done by your doctor to test for Type 1 or Type 2 diabetes or gestational diabetes. If you are a pregnant woman being tested for gestational diabetes, the liquid you must drink will have less sugar (glucose) dissolved in water. Shown below is a Blood Sugar Level Chart, simply designed for basic glucose and blood sugar testing. For more nutritional information, charts, health stats, worksheets, and other free printable items, visit any of the links shown on this page.
Click this link to exit the Blood Sugar Level Chart page, and visit the Main Health Info Page.Hit this link for a collection of Great American Recipes. If its a big enough collapse you’ll have shortness of breath and could lose consciousness if you then exerted yourself. Rejuvenating pancreatic cells – Yoga postures that aid relaxation (asanas) stretch the pancreas which can stimulate the production of insulin-producing beta cells. Prescribed drugs such as steroids and all different types of insulin reproductive hormones may also be causes but less research has been done in these fields to give definitive answers. I can see no reason to recommend the VERT to anyone except possibly in unusual Diabetes Nutrition For Elderly and unlikely cases of people wanting to juice very particular things that the VERT may excel at in terms of convenience at least if not juice quality (such as being able to juice cherries with the pits). A Multi-Center Placebo-Controlled Double-Blind Study to Confirm the Reversal of Hepatorenal Syndrome Type diabetic sweet potato cake recipes Diabetes Acute Lung Injury and the Anti-inflammatory Effects of Thiazolidinediones.
Insulin injections are executed making use of a disposable syringe and needle and it is vital for the individual to know how to render the therapy properly. Science, Technology and Medicine open access publisher.Publish, read and share novel research.
The Effects of Glucocorticoids on Fetal and Placental DevelopmentEmin Turkay Korgun1, Asl? Ozmen1, Gozde Unek1 and Inanc Mendilcioglu2[1] Akdeniz University, Medical Faculty, Histology and Embryology Department, Antalya, Turkey[2] Akdeniz University, Medical Faculty, Obstetrics and Gynecology Department, Antalya, Turkey1. The Diabetes Forum - find support, ask questions and share your experiences with 209,001 people.
HbA1c refers to glycated haemoglobin (A1c), which identifies average plasma glucose concentration. When the body processes sugar, glucose in the bloodstream naturally attaches to haemoglobin.
The amount of glucose that combines with this protein is directly proportional to the total amount of sugar that is in your system at that time. Because red blood cells in the human body survive for 8-12 weeks before renewal, measuring glycated haemoglobin (or HbA1c) can be used to reflect average blood glucose levels over that duration, providing a useful longer-term gauge of blood glucose control. If your blood sugar levels have been high in recent weeks, your HbA1c will also be greater.
Note that this is a general target and people with diabetes should be given an individual target to aim towards by their health team.
An individual HbA1c should take into account your ability to achieve the target based on your day to day life and whether you are at risk of having regular or severe hypos. HbA1c provides a longer-term trend, similar to an average, of how high your blood sugar levels have been over a period of time.
An HbA1c reading can be taken from blood from a finger but is often taken from a blood sample that is taken from your arm. Blood glucose level is the concentration of glucose in your blood at a single point in time, i.e. This is measured using a fasting plasma glucose test, which can be carried out using blood taken from a finger or can be taken from a blood sample from the arm. However, fasting glucose tests provide an indication of your current glucose levels only, whereas the HbA1c test serves as an overall marker of what your average levels are over a period of 2-3 months. HbA1c is a measure of how well controlled your blood sugar has been over a period of about 3 months. Some people may be set less challenging targets by their doctor, particularly where hypoglycemia is a concern.
Everyone with diabetes mellitus in the UK should be offered an HbA1c test at least once a year. Although HbA1c level alone does not predict diabetes complications, good control is known to lower the risk of complications.
It is important to note that because blood glucose levels fluctuate constantly, literally on a minute by minute basis, regular blood glucose testing is required to understand how your levels are changing through the day and learning how different meals affect your glucose levels. Find support, ask questions and share your experiences with 209,001 members of the diabetes community.
10 week (free) low-carb education program developed with the help of 20,000 people with T2D and based on the latest research. The first comprehensive, free and open to all online step-by-step guide to improving hypo awareness. Currently almost 1 in every 3 Fijians is being diagnosed with diabetes, that’s 30% of the population. You can always visit your nearest diabetes hub to get your sugar checked ad learn how to stay in control of your diabetes. They can check your blood glucose (sugar) levels there and assess any symptoms you may have.
Glycated hemoglobin is a substance in red blood cells that is formed when blood sugar (glucose) attaches to hemoglobin. How the Test is Performed Blood is drawn from a vein, usually from the inside of the elbow or the back of the hand. And when our bodies give out we would diabetes management lifestyle offer them to the earth and return the favor we have received as we ate our way through life.
Also on both if you are doing well you start getting super hard questions making you feel like your failing. I have read The Face On Your Plate by Jefferey Masson The Kind Diet by Alicia Silverstone and various easy diabetic menus media across the internet depicting the sad state that the food industry is in. Obviously if Diabetes Nutrition For Elderly there is physical or emotional abuse the partner should be encouraged to separate and reassess and if there are children involved they must be removed from the house if they are being endangered emotionally or physically. Peculiarities of the endocrine diabetes wristbands color time structure in noninsulin-dependent adult-onset (type II) diabetes mellitus. While those are the top three early warning signs of diabetes there are others that could indicate a constant high blood sugar. Glucocorticoids might show their effects on angiogenesis mechanisms by altering intracellular signal transduction pathways. Effect of glucocorticoid overexposure on GLUT1 and GLUT3 expression in placental endothelial cells.
IntroductionGlucocorticoids(GCs), steroid hormones produced predominantly by the adrenal gland, are key mediators of stress responses.
This guide explains what HbA1c is, how it differs from blood glucose levels and how it's used for diagnosing diabetes. It develops when haemoglobin, a protein within red blood cells that carries oxygen throughout your body, joins with glucose in the blood, becoming 'glycated'. It essentially gives a good idea how high or low, on average, your blood glucose levels have been. This may be more likely if you have recently had your medication changed or your health team are otherwise wishing to monitor your diabetes control more than once a year. Type 2 diabetes is more common than Type 1, it is also more easily avoided if the correct healthy lifestyle is adopted. However, some people with Type 2 diabetes have symptoms so mild that they go unnoticed so it is always best to get your blood sugar levels tested by a medical professional.
Diabetes Nutrition For Elderly algorithm for gestational diabetes management type 2 diabetes a1c goal There are many different types of oral medications available to treat type 2 diabetes. He meets the other somewhat unusual inhabitants of the Key and takes up painting but soon finds that the painting may be controlled by forces beyond his control.
Factors such as insulin resistance and rapid metabolism of insulin in dogs may necessitate a change in dose or insulin preparation. Put the nylon stocking on 3 months ago and about 30 loads later stilldoing the job well without having to change it. Simply fill out your name and email below That’s the only way I can rate this product. In physiological conditions; in the case of moderate GC concentrations (left picture), vascular homeostasis is tightly regulated.
Whilst the acute and chronic effects of pharmacological glucocorticoid excess are well-recognized (including induction of hyperglycemia, insulin resistance, hyperlipidemia, hypertension and dysphoria, with suppression of immune, inflammatory and cognitive processes), their role in the biology of the response to stress is more nuanced, with balanced homeostatic effects to facilitate short-term survival and recovery from challenge [1, 2]. Over the next few hours, your doctor will test the sugar in your blood again and check your numbers against standard numbers. The health care provider wraps an elastic band around the upper arm to apply pressure to the area and make the vein swell with blood. Next, the health care provider gently inserts a needle into the vein. Your name may need to be listed on a sitagliptin pregnancy registry when you start using this medication. Types of Insulin Insulin Resistance Therapy Combined Insulin and Oral Treatment Regimes Practical Aspects. VEGF, VEGFR1&R2 expression, angiogenic cytokine production, endothelial cell migration, blood flow velocity etc… is maintained in a balance in functional endothelial cells.
In addition, glucocorticoids play an essential role in normal fetal development and are important for the development and maturation of various fetal tissues including the liver, lungs, gut, skeletal muscle and adipose tissue in preparation for extrauterine life. That’s terrible…Was there a problem with your Diabetes Nutrition For Elderly application? Insulin resistance is a common problem in women with PCOS often leading to diabetes and obesity.
A dietitian in a diabetes center or some hospitals and outpatient clinics may be required to be a CDE.


But when GC concentration is increased (right picture), endothelial cell are subjected to excess GC.
As a result of GC overexposure GLUT1 and GLUT3 mRNA and proteins are increased in placental endothelial cells. Glucocorticoids most notably act during late gestation to stimulate surfactant production by the lung. The following article gives information Diabetes Nutrition For Elderly about diabetes and what causes diabetes.
I feel great and am only disappointed that a dude telling me I was too fat to be seen in public with him is what it took for me to start taking control of my body. Left panel refers possible physiological conditions and right panel refers effects of GC overexposure on GLUTs. This action is critical to prepare the fetus for extrauterine life, and it is for this reason that synthetic glucocorticoid treatment is so widely used in preterm pregnancies where lung immaturity threatens neonatal viability. Once the blood has been collected, the needle is removed, and the puncture site is covered to stop any bleeding. In infants or young children, a sharp tool called a lancet may be used to puncture the skin and make it bleed. I think if this is your diabetes guidelines medications motivation you should really reconsider medicine.
Although these treatments greatly improve survival [3], they are not without adverse effects.Glucocorticoids regulate many of the processes required for successful embryo implantation, as well as for the subsequent growth and development of the fetus and placenta.
The blood collects into a small glass tube called a pipette, or onto a slide or test strip. It has been shown that glucocorticoids have several roles in improving the intrauterine environment. Afterward, there may be some throbbing. Why the Test is Performed Your doctor may order this test if you have diabetes.
For example, in uterus, glucocorticoids regulate the synthesis of prostaglandins that have been implicated to play critical roles during implantation by increasing stromal vascular permeability [4] and in the initiation of parturition [5]. The peri-implantation secretion of human chorionic gonadotrophin (hCG) from human term trophoblasts can be stimulated by up to 10-fold by treatment for 24 to 72 h with synthetic glucocorticoids dexamethasone and triamcinolone [6, 7]. In first trimester human cytotrophoblasts, cortisol can suppress the synthesis of the pro-inflammatory interleukin (IL)-1b [8]. Similarly, in term human placental cytotrophoblasts, physiological concentrations of cortisol and numerous synthetic glucocorticoids can inhibit secretion of pro-inflammatory cytokines tumor necrosis factor (TNF)-?, IL-6 and IL-8 without affecting the expression of anti-inflammatory cytokine IL-10 [9-11].
However, you and your health care provider must decide what is a normal HbA1c level for you. Normal ranges may vary slightly among different laboratories. Glucocorticoids contribute to preventing immunological rejection of the fetal semiallograft in the pregnant uterus by inhibiting eosinophil infiltration [12].
Talk to your doctor about the meaning of your specific test results. What Abnormal Results Mean Abnormal results mean that your blood glucose levels have been above normal over a period of weeks to months. Moreover, glucocorticoids profoundly and specifically suppress expression of fibronectin and laminin, two extracellular matrix proteins that are important mediators of uterine–placental adherence [6].Furthermore, glucocorticoids activate many of the biochemical processes in these tissues such as altering expression of numerous receptors, enzymes, ion channels, transporters, growth factors, cytoskeleton proteins, binding proteins, clotting factors, gap and tight junction proteins and intracellular signaling pathways’ components involved in growth. If your HbA1c is above 7%, it means that your diabetes control may not be as good as it should be. High values mean you are at greater risk of diabetes complications.
Taken together, these glucocorticoid-induced changes in cell physiology combine to produce functional alterations at the systemic level [13].In pregnancy, glucocorticoid administration is used mainly in the management of women at risk of preterm labor and in the antenatal treatment of fetuses at risk of congenital adrenal hyperplasia. If you can bring your level down, you decrease your chances of long-term complications. Ask your doctor how often you should have your HbA1c tested.
It is recommended that, for pregnant women who are at risk of preterm delivery within 7 days between 24 weeks and 34 weeks of gestation, a single course of corticosteroid administration should be performed. Usually, doctors recommend testing every 3 or 6 months. Risks Veins and arteries vary in size from one patient to another and from one side of the body to the other. And a single course of antenatal corticoids should be administered to women with premature rupture of membranes before 32 weeks gestation to reduce the risks of respiratory distress syndrome, perinatal mortality and other morbidities [14]. Numerous evidence indicates that increased exposure of the fetus to glucocorticoids in mid- to late pregnancy may result in adverse outcomes including intrauterine growth restriction (IUGR) [15-18], postnatal hypertension [15, 19], postnatal cardiovascular disease [20], postnatal glucose intolerance [20], increased postnatal activity in the hypothalamo–pituitary–adrenal axis [21-24], effects on fetal brain development [21, 25, 26]. On hormone binding, activated GR translocates from the cytoplasm to the nucleus as a dimer to associate with specific DNA sequences termed glucocorticoid response elements (GREs) and acts as a ligand-dependent transcription factor [28]. GRs are highly expressed in decidua, chorion, amnion, stromal fibroblasts, vascular smooth muscle cells and endothelial cells of human term placentas, with moderate expression in cytotrophoblasts and negligible expression in syncytiotrophoblast [30-34].
Because the significance of glucocorticoids to the early mammalian embryo is clear and glucocorticoid action within the cell is regulated by GR, we investigated GR expression during the course of rat embryogenesis until day 12 of gestation. The demonstrated ontogenetic pattern of GR expression indicates the potential sites of biological action of the glucocorticoids, providing supportive evidence for its critical importance during the course of embryogenesis in rats [35]. The intracellular enzyme 11?-hydroxysteroid dehydrogenase (11?-HSD) catalyzes the interconversion of bioactive glucocorticoids (cortisol and corticosterone) and their inactive metabolites (cortisone and 11-dehydrocorticosterone).
Thus, it is an important modulator of glucocorticoid bioavailability in both glucocorticoid and mineralocorticoid target organs [36].
In placenta, 11?-HSD1 protein is expressed specifically in the placental villous endothelial cells, amnion, chorionic and extravillous trophoblasts(EVTs).
As the placenta differentiates, there is an up-regulation in the expression of 11?-HSD2 enzyme that becomes the major placental isoenzyme [40]. 11?-HSD2 protein is localized exclusively in the syncytiotrophoblast and invasive extravillous trophoblasts with no expression in the chorion or amnion [41-43]. The distinct pattern of 11?-HSD1 and -2 localizations may indicate having different physiological functions. In normal pregnancy, maternal glucocorticoid levels are markedly higher than those in the fetal circulation.
It has been stated that the role of placental 11?-HSD is to protect the fetus from adverse effects of maternal glucocorticoids. 11?-HSD2 is better suitable for this role because of its location (the site of maternal–fetal exchange) and its enzymatic properties (higher affinity for cortisol).
This enzyme acts as a ‘barrier’ to prevent premature or inappropriate action at glucocorticoid-responsive tissues during fetal development [44]. It has been suggested that a reduction in the expression or activity of placental 11?-HSD2, by leading to increased transplacental passage of active glucocorticoids, reduces fetal growth. Numerous studies have shown that inhibition of 11?-HSD2 during pregnancy leads to a reduction in birth weight and the development of later hypertension and glucose intolerance [46-48], as well as programming increased HPA axis activity and anxiety-related behaviors [49]. Moreover, placentas from 11?-HSD2 knockout mice fetuses have impaired labyrinth zone capillary development accompanied by a decline in vascular endothelial growth factor (VEGF)-A mRNA expression and altered transport of nutrients by system A amino acid transporter (SNAT) [50].
Furthermore, a correlation between decreased activity of 11?-HSD2 in the human placenta and IUGR has been reported [15, 51, 52].
In addition, mutations in the HSD11B2 gene in humans, although rare, markedly reduce birth weight [53]. It was found that while maternal administration of glucocorticoids caused IUGR, glucocorticoid administration directly into the fetal circulation did not restrict fetal growth, which suggests that the growth limiting effects of glucocorticoids are mediated via actions in the utero-placental unit rather than effects on fetal tissues [54]Placental development is a critical determinant of fetal growth and glucocorticoids affect growth and development of the fetus indirectly by affecting placental development and function.
The actions of glucocorticoids on fetal growth are mediated, in part, by changes in the placenta.
In sheep, rats, mice and non-human primates, administration of synthetic glucocorticoids during late gestation reduces placental weight.
In most of these species, the effect of glucocorticoids on the placenta is greater than that on the fetus [13]. These findings suggest that glucocorticoids stimulate syncytiotrophoblast differentiation and maturation [55-57]. Microarray analysis showed that maternal glucocorticoid administration leads to marked changes in the gene expression profile in the placenta.
Dexamethasone (Dex) caused a decrease in expression of genes involved in cell division such as cyclins A2, B1, D2, CDK 2, CDK 4 and M-phase protein kinase along with growth-promoting genes such as epidermal growth factor receptor, bone morphogenetic protein 4 and insulin-like growth factor-binding protein 3.
In addition, Dex treatment led to down-regulation of genes involved in protein biosynthesis, skeletal development, and collagen metabolism. There was also decreased expression of genes involved in cell division, DNA replication, chromosome segregation, DNA alkylation, nucleotide and nucleoside biosynthesis, microtubule-based processes, B-cell activation and differentiation processes, innate immune response, antigen processing and presentation, and complement system [58].
Treatment of rats with glucocorticoids restricts placental vascular development via inhibition of the VEGF-A and peroxisome proliferator-activated receptor ? (PPAR?) which is regulated by VEGF-A expression [59, 60].
In addition, in response to glucocorticoid treatment of either the mother or fetus, there are changes in the placental handling of certain amino acids such as alanine, glutamine and glutamate. However, there have been few studies on the effects of glucocorticoids on amino acid transporters in the placenta of any species to date [61, 62]. Additionally, glucocorticoids change the production and metabolism of hormones by the placenta such as prostaglandins, placental lactogen, leptin, corticotrophin-releasing hormone (CRH), estrogens, progesterone and other progestagens [63, 64]. Glucocorticoids also alter the placental activity of various enzymes involved in the synthesis and inactivation of steroids and thyroid hormones such as 17,20-lyase, 17?-hydroxylase, aromatase, renin and endothelial nitric oxide synthase [63].
The effects of glucocorticoids on placental cell cycleGlucocorticoids play a fundamental role in pregnancy with effects on decidualization, implantation, placental development, fetal brain development, lung maturation and parturition but fetal-placental exposure to maternally administered glucocorticoids may lead to abnormalities of fetal and placental growth [15, 19, 65]. The mode of action of glucocorticoids in placental growth inhibition has not been determined. Human placental development is established by trophoblast invasion into the uterine endometrium and its vasculature. The resulting changes will facilitate an increase in intervillous blood flow and, hence, the exchange of nutrients and molecules between maternal and fetal blood. The transports as well as metabolic and endocrine functions of the placenta reside primarily in the floating villi covered by the syncytiotrophoblast, a tissue that results from terminal differentiation of underlying villous cytotrophoblasts and their subsequent fusion. Anchoring villi establish physical connection of the placenta with the decidua predominantly by a subpopulation of cytotrophoblasts known as EVT. Both villous and extravillous cytotrophoblast subpopulations arise by proliferation and differentiation from stem cells located within the cytotrophoblast layer of the chorionic villi [66].On the basis of the immunostaining of the Ki67 antigen, a cell cycle regulator with yet unknown role, EVTs have been categorized as the proliferative phenotype, which is primarily located in the proximal part, and the invasive phenotype that is located mainly in the distal part of cell columns [66]. Current understanding assumes that EVT can differentiate, thereby acquiring an invasive phenotype, which eventually enables them to invade the maternal decidua and spiral arteries. Thus placental development involves proliferation and differentiation of the cytotrophoblasts in a manner that is tightly regulated in time and space.Eukaryotic cell cycle consists of four phases, G1, S, G2 and M. G1 and G2 are preparation phases for DNA synthesis (S) and mitosis (M) phases respectively. During G1 and G2 phases cell growth, doubling of the amount of protein and organelles and preparation for the next phase occurs. If the conditions are not appropriate, cells in G1 phase stop cell cycle progression and enter into a resting state, known as G0 phase, where they continue biological functions but do not go through the rest of the cell cycle. When growth signals are received, cells in G0 phase can continue the cycle through the G1 phase [67, 68].The eukaryotic cell cycle is regulated by the coordinated activity of a family of cyclin-dependent kinases (CDKs). These are positively and negatively regulated by the cyclin and CDK inhibitor families [69, 70]. Based on the timing of their appearance in the cell cycle, cyclins can be divided into two groups, i.e.
A few studies localized cell cycle regulators that are specifically expressed during key transitions and phases [81-83].The hypothesis that the coordinated expression of cell cycle progression and inhibition factors will determine whether cytotrophoblasts proliferate or undergo cell cycle arrest or cell cycle exit allowing subsequent differentiation was tested by our team. The cell cycle promoters cyclin A, cyclin B1, proliferating cell nuclear antigen (PCNA), Ki67 and the cell cycle inhibitors p21, p27 and p57 were immunolocalized in tissue sections of first trimester pregnancies (weeks 6 and 9-12). Villous cytotrophoblasts were immunolabelled for Ki67 and cyclin A but only few were stained with anti-cyclin B1.
The syncytiotrophoblast was devoid of immunoreactivity for any of the cell cycle progression factors. It expressed especially p21, whereas p27 and p57 were predominantly found in villous cytotrophoblasts. PCNA, Ki67, cyclin A and cyclin B1 were immunolocalized in proximal and distal EVTs of anchoring villi and in EVT which had invaded the upper decidual segments. These data clearly suggest different functions for p21, p27 and p57 in placental development with distinct roles for p21 and p57 in syncytiotrophoblast and EVT differentiation, respectively. The results may also challenge the concept of differential mitotic activity in the proximal and distal parts of the first trimester cytotrophoblast cell column, but more functional studies are clearly needed.


Schematic representation of our immunohistochemistry results in the rat placenta is showed in Figure 2.
We investigated the spatial and temporal immunolocalization of PCNA, Ki67, p27 and p57 in normal and Dex-induced IUGR placental development in pregnant rats. PCNA immunolabeling intensity in placentas of the control group was statistically significantly higher than that in the Dex-induced IUGR group placentas on all days in junctional and labyrinth zones (JZ and LZ, respectively). We observed decreased Ki67 staining intensity in the labyrinth trophoblasts of Dex-induced IUGR placentas compared to controls on day 21. Ki67 immunolabeling intensity was higher in the control group than that in the IUGR group placentas on all days in both zones except for day 21 in the junctional zone. These differences were statistically significant on days 15, 17 and 19 in the junctional zone and on days 13, 15, 17 and 21 in the labyrinth zone. Ki67 staining intensity decreased gradually after day 15 in both zones of control and IUGR placentas. Ki67 immunostaining intensities were stronger in the labyrinth zone compared to the junctional zone in both groups.
Moreover, after day 17, scarcely any Ki67 immunostaining was obtained in the IUGR placentas in the junctional zone. We found stronger p27 immunolabeling intensity in Dex-induced IUGR placentas when compared to control placentas in both junctional and labyrinth zones for all gestational days (Table 1) [89].
In accordance with this, in another study, it was observed that in the Dex-induced human choriocarcinoma JEG-3 cells p27 mRNAs were upregulated [90].
We observed that p57 immunostaining intensities in Dex-induced IUGR placentas were stronger compared to controls in both zones for all gestational days. Akt activation was significant at junctional zones of the rat placenta, especially at spongiotrophoblast cells and giant cells, and reduced after dexamethasone treatment. In another study, decreased levels of placental Akt phosphorylation was observed after in utero exposure to Dex [92].Antenatal Dex use is associated with reduction in fetal and placental weight with morphological changes in the placenta. Dex-treated mouse placentas showed swollen trophoblast cells in both the junctional and labyrinth zones and increased apoptosis of trophoblast cells in the junctional zone. Increasing antenatal corticosteroid exposure was associated with villous fibrosis, stromal mineralization, and less frequent villous infarction [93].
In addition, treatment with Dex prevented the normal rise in VEGF expression and the associated increase in labyrinthine vascularity over the final third of pregnancy. Therefore, Dex appears to reduce labyrinth zone growth by preventing the normal development of the fetal vasculature within the labyrinth zone [59]. Moreover, microarray analysis showed that Dex caused a decrease in expression of genes involved in cell division such as cyclins A2, B1, D2, CDK 2, CDK 4 and M-phase protein kinase along with growth-promoting genes such as epidermal growth factor receptor, bone morphogenetic protein 4 and insulin-like growth factor-binding protein 3 [58].
Impaired growth in Dex-treated placentas was also characterized by decreased expression of both prolactin-like protein-B and insulin-like growth factor (IGF)-II, particularly in the junctional zone of the rat placenta [92]. Dex-induced trophoblast apoptosis was mediated through activation of caspases 1 and 3 [58, 95]. Apoptosis was also induced in primary cultures of third trimester human decidual cells when treated with cortisol, cortisone, or dexamethasone [34]. These findings suggest that Dex stimulates syncytiotrophoblast differentiation and maturation [57]. In another study, BeWo and JEG-3 choriocarcinoma cell lines used as models for human trophoblast were cultured with another synthetic glucocorticoid triamcinolone acetonide (TA). TA altered the number of viable and dead cells as well as cyclin B1 expression levels shown by Western blotting and to a lesser extent, invasion of BeWo and JEG-3 cell lines determined by Matrigel invasion assay and by measuring the secretion (ELISA) of matrix-metalloproteinases (MMP-2, MMP-9) [97]. The effects of glucocorticoids on fetal and placental angiogenesis mechanismsAngiogenesis is a complex process that may be initiated by a large number of stimuli and that is performed through multiple biologic pathways and a variety of molecules. With the increased understanding of angiogenesis, it has become clear that many of its pathways are parallel and redundant, greatly complicating efforts to interrupt the process. The disruption of one pathway most likely does not abolish completely the formation of new blood vessels, which may explain the less than perfect clinical results achieved when treating neovascular processes with currently available regimens. Combination therapies and drugs that target more than one pathway have become more popular and intensively explored.Angiogenesis is required for the cyclic processes of endometrial growth, breakdown, and repair during the menstrual cycle, and it provides a richly vascularized tissue receptive for implantation and placentation [98]. The dosages and types of glucocorticoids changes depending on the severity of the symptoms and treatment procedure [99]. Endothelial cells are seem to be a target of glucocorticoid effect as they both express glucocorticoid and mineralocorticoid receptors [101, 102]. But overexposure to glucocorticoids during pregnancy has adverse effects on placental angiogenesis mechanisms. They showed that treatment with dexamethasone prevented the normal rise in VEGF expression as a LZ specific manner. Their data suggest that glucocorticoid induced restriction of fetal and placental growth is mediated, in part, via inhibition of placental VEGF expression and associated reduction in placental vascularization. Therefore, dexamethasone appears to reduce LZ growth by preventing the normal development of the fetal vasculature within the LZ.
As it is mentioned in the study above, GCs have adverse effect on placental angiogenesis mechanisms.
This effect would be related with both angiogenic activity of the endothelial cells or maybe related with proliferation or cell survival processes. It was reported in a previous study that GCs inhibit tube formation of cultured endothelial cells [103] but the molecular mechanisms underlying this effect hasn’t been clearly understood [104]. This investigation addressed the hypothesis that the potent antiangiogenic action of glucocorticoids is due to prevention of tube formation by endothelial cells.
Cultured human umbilical vein endothelial cells (HUVEC) and aortic endothelial cells (HAoEC) were used to determine the influence of glucocorticoids on tube-like structure (TLS) formation, and on cellular proliferation, viability and migration. Dexamethasone or cortisol (at physiological concentrations) inhibited both basal and prostaglandinF-2? -induced and VEGF stimulated TLS formation in endothelial cells cultured on Matrigel, effects which were blocked with the glucocorticoid receptor antagonist RU38486. Time-lapse imaging showed that cortisol blocked VEGF-stimulated cytoskeletal reorganization and initialization of tube formation. Exposureto glucocorticoids reduced the formation of cell-cell contacts rather than increasing degradation of existing tubes. They concluded that glucocorticoids interact directly with glucocorticoid receptors on vascular endothelial cells (ECs) to inhibit TLS formation.
This action, which was conserved in ECs from two distinct vascular territories, was due to alterations in cell morphology rather than inhibition of EC viability, migration or proliferation.
These findings provide important insights into the anti angiogenic action of endogenous glucocorticoids in health and disease [105].According to the results of an ongoing study of us, Triamcinolone treatment decreased VEGF expression in HUVECs. In this study, we tested the hypothesis that IUGR could be observed in fetuses as a result of insufficient nutrient transport depending on the glucocorticoid effect on placental angiogenesis mechanism that leads to inadequate vessel development.
RT-PCR and Western blot analyses were performed on placentas while ELISA test was applied to sera and HUVEC culture media.
We found that in HUVECs; VEGF, VEGFR1, VEGFR2, Placental Growth Factor (PIGF) and Fibroblast Growth Factor (FGF) gene levels on 48 and 72 hours decreased in 50 mM TA groups compared to control. VEGFR1 protein quantity decreased and VEGFR2 protein quantity increased in a dose- and time-dependent manner. According to ELISA results, VEGFR1 secreted by HUVEC cells decreased while VEGFR2 and FGF increased. In Matrigel experiments, decreased vessel tube structures were created by HUVEC cells exposed for 72 hours to 50 mM TA. The amount of VEGF in Dex treated rat sera statistically significantly decreased on days 14, 16 and 20, while there is no difference on day 18 compared to control.
VEGF protein amount showed a decrease in all gestational days of IUGR group compared to control in rat placentas. VEGFR1 decreased in advancing pregnancy days of control group while increased in parallel to pregnancy days of IUGR group.
VEGF and VEGFR1 gene level was lower at term rat placentas compared to control group at gestational day 20. It was observed that, the IUGR group had significantly smaller embryos on day 20 of gestation and had smaller placentas on day 14, 16, 18 and 20 compared with control.
Maternal dexamethasone treatment led to a significant decrease in Akt activation on day 16, 18, and 20. We observed that phospho-Akt immunolabelings were remarkable in junctional zone in control groups and weaker in IUGR groups. Therefore, dexamethasone induced decreased Akt phosphorylation may negatively affect the placental angiogenesis mechanisms. These studies report that GCs alter the physiological condition of the vasculature and leads pathological conditions. In conclusion, maternally administered betamethasone produces a consistent decrease in several indices of placental eNOS function that may play a role in the altered cardiovascular dynamics and fetal growth retardation produced by betamethasone administration in late pregnancy.
Hormones regulate blood vessel growth by controlling the production of local chemical mediators, often other hormones, but also growth factors, cytokines, enzymes, receptors, adhesion molecules, and metabolic factors.
As mentioned above, GCs may show their effects directly on endothelial cells or indirectly for example by altering cytokine production that may affect placental vasculature. The dose effect of glucocorticoids on cytokine (TNF-?, IL-6 and IL-10) production was examined using ELISA. There was a stepwise reduction of TNF-? and IL-6 with increasing doses of betamethasone and methyl-prednisolone from placentas of women with preeclampsia and normal pregnancy. However, IL-10 was not altered in conditioned medium by increasing doses of glucocorticoids. In pregnancy, TNF-? can cause direct damage to endothelial cells, increase endothelial cell permeability, up-regulate endothelial adhesion molecules (ICAM-1, VCAM-1, E-Selectin) and promote vasoconstriction, all of which are identified in the pathogenesis of preeclampsia [113].
IL-10 is an immunosuppressive Th2-type cytokine which is produced by immune cells including T-cells, monocytes, macrophages, granulocytes and NK cells and also trophoblasts. IL-10 has been also shown to be a potent inhibitor of Th1 cell proliferation and the production of Th1-type cytokines such as TNF-? [114]. To observe the influence of maternal betamethasone administration for fetal lung maturation on the arterial, venous and intracardiac blood flow of the fetus and the uterine arteries; twenty-seven women with singleton pregnancies were examined before the first, and 30 min and 8, 24, 48 and 72 h after the second of two single doses of 8 mg of betamethasone. The blood flow velocity waveforms of the umbilical artery (UA), the middle cerebral artery, the uterine arteries, the ductus venosus, the inferior vena cava and the right hepatic vein, the pulmonary trunk, the ductus arteriosus and the right and left intraventricular inflow of the heart was recorded.
The resistance index of the UA showed a significant transient decrease 30 min after the second betamethasone dose.
The peak systolic velocity of the ductus arteriosus increased significantly 30 min after the 2nd dose and then returned to non-significant values. However, this effect seems to be mild and reversible and does not appear to contraindicate the use of corticosteroids to promote fetal lung maturation [115].
Therefore, it could be mentioned that long term dexamethasone usage my result with decreased maternal blood velocity which would negatively affect angiogenesis mechanisms as maternal blood itself contains angiogenesis related proteins.It is reviewed by Oliver et al.
Angiostatic steroids have been proposed to inhibit angiogenesis by altering the capillary basement membrane composition, suppressing its dissolution, and inhibiting endothelial cell migration, in addition to their capacity of regulating the participation of in?ammatory cells in the neovascular process [122-124].
There is a growing body of evidence that reports inhibitive effects of glucocorticoids on angiogenesis mechanisms [105, 125-128] but there is limited data about the impact of glucocorticoids on placental angiogenesis mechanisms. Glucocorticoid-mediated inhibition of angiogenesis is important in physiology, pathophysiology and therapy.
However, the mechanisms through which glucocorticoids inhibit growth of new blood vessels have not been established. The effects of glucocorticoids on placental glucose transportersThe Glut protein family belongs to the Major Facilitator Superfamily (MFS) of membrane transporters [129].



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