Gonads and placental hormones in gestational diabetes
The placenta is also a major endocrine organ being responsible for synthesizing vast quantities of hormones and cytokines that have important effects on both maternal and fetal physiology [ 19 — 22 ]. As a gateway to the fetus the placenta is affected by numerous environmental factors including nutrient status and tissue oxygenation, which may modify epigenetic marks and gene expression within the placenta and therefore placental development and function [ 23 — 25 ].
Studies of rodents and large animals have shown placental development to be highly adaptable, with many means of compensating for poor nutritional conditions [ 26 — 30 ]. Sex differences in the rate of fetal growth have long been recognized [ 31 ]. The sex of the embryo affects the size of both the fetus and the placenta, together with the ability of the placenta to respond to adverse stimuli [ 27 , 32 , 33 ].
The placenta has traditionally been considered an asexual organ and therefore, many studies focusing on the placenta have not taken the sex of the embryo into account [ 33 ]. But given its extraembryonic origin, the placenta has a sex: that of the embryo it belongs to [ 33 — 35 ] and numerous DOHaD studies indicate that sex differences can originate early in development and in particular in the placenta [ 36 ].
Studies by Ishikawa et al. Although the possession of one X chromosome rather than two leads to an increase in placental size, the underlying mechanism is still to be determined [ 37 ]. In mice and cattle, accelerated development is already evident in XY blastocysts; cell division among male embryos occurs more rapidly than in female embryos [ 38 ] and, in humans, boys grow more rapidly than girls from the earliest stages of gestation [ 39 ]. These differences may start as early as the blastocyst stage in bovines: one third of genes showed sex differences in gene expression [ 40 , 41 ].
Gene expression analysis either for candidate genes or at the genome-wide level show that both the trajectories under basal conditions and those modulating responses differ between the sexes [ 15 ]. Analysis of genes involved in amino acid transport and metabolism identified sex differences both in average placental gene expression between male and female and in the relationships between placental gene expression and maternal factors [ 42 ].
Ontological analysis of such data suggests a higher global transcriptionnal level in females and greater protein metabolism levels in males. Specifically global glucose metabolism and pentose-phosphate pathway activity are twice and four times greater in bovine male vs.
At birth, placental weights and FPI fetus-to-placenta weight ratio index, reflecting placental efficiency , tend to be greater in boys than girls [ 44 ]. These observations suggest that males may be both more responsive to growth promoting influences, and more susceptible to supply disturbances [ 44 , 45 ].
How could placental sex-specific functions under basal conditions, and sex-specific sensitivity to environmental conditions contribute to the differences in frequency, severity and age at onset of NCDs between the sexes? Unequal gene expression by the sex chromosomes between males and females play an important role even before implantation and the initiation of adrenal and gonad development.
The burgeoning field of epigenetics provides credible molecular mechanisms to account for gene expression alterations that may persist in the long term. The resulting changes in epigenetic marks may alter cell fate decisions, the ensuing growth and development of tissues and organs, and subsequently be responsible for inadequate responses to later challenges such as an obesogenic environment in a sex-specific manner [ 15 , 47 , 48 ].
The aim of this review is to discuss the emerging knowledge on the sex-specific relationships between diverse environmental influences on placental functions and the risk of disease later in life. Given the abundance of X-linked genes involved in placentogenesis, and the early unequal gene expression by the sex chromosomes between males and females, this review focusses on the role of X- and Y-chromosome-linked genes, and especially on those involved in the peculiar placenta-specific epigenetics processes, giving rise to the unusual placenta epigenetic landscapes.
Sex-specific outcomes of the effects of placental growth on fetal programming As a critical messenger between the maternal environment and the fetus, the placenta may play a key role not only in buffering environmental effects transmitted by the mother but also in expressing and modulating effects due to preconceptional exposure of both the mother and the father to stressful conditions.
Figure 1 shows how such influences may operate on the transmission of environmental influences to subsequent generation s , and illustrate the central role of the placenta on the sex-specificity of these parent-of-origin effects. Support for the possibility of inter and transgenerational effects are also emerging, making it important to know the role played by the placenta and the possible maternal and or paternal epigenetic imprints carried by the gametes forming the zygote.
Indeed, maternally or paternally transmitted non-erased epigenetic alterations of key developmental genes may perturb early trophoblast development in a sex-specific manner Figure 1. Figure 1 Sex-specific transmission of exposure to environment to subsequent generations.
Environmental factors - including nutrition, psychosocial stress, toxins, endocrine disruptors, tobacco, alcohol, microbiota — impact individual F0 epigenetic landscapes hence gene pathways and networks in ways that differ between the sexes.
For example maternal and paternal preconceptional exposures can modify gamete quality and be transmitted to the subsequent F1 generation. Additionally consequences of maternal F0 exposure during pregnancy stress, metabolism, diet, hormonal changes… can be transmitted from the maternal to the fetal compartment via the placenta in a sex-specific manner and affect F1 tissue development.
Programming of somatic tissues can lead to changes in long-term health outcomes in the first generation. Moreover, primordial germ cells, which develop and undergo reprogramming during fetal development, can also be affected by F0 maternal environment and contribute genetic and epigenetic information to the F2 generation. Maternal and paternal lineages affect the transmission of such influences differently. In particular, multigenerational exposure on the maternal lineage can be seen in the F0, F1 and F2 generations, and transgenerational phenotype would be observed in F3, whereas on the paternal lineage multigenerational exposure concerns F0 and F1, and transgenerational phenotype in F2 and F3 generations.
Full size image There is evidence to suggest that not only maternal mal- or undernutrition in the context of famines [ 20 , 49 ], maternal overnutrition, gestational diabetes or obesity, maternal stress or depression, but also environmental stressors such as drugs [ 50 ] and endocrine disruptors [ 51 ] are deleterious to the health of the offspring. Many of these factors have been shown to have the same range of defects and lead to the development of the metabolic syndrome [ 52 — 56 ], or mental health disorders in the offspring [ 57 , 58 ] with striking sex-specificity [ 15 , 59 — 63 ].
Two common complications of pregnancy, pre-eclampsia and asthma, have provided valuable insight into the way in which the feto-placental unit influences maternal physiology in a sex-specific manner. There is also growing evidence to suggest that some of these changes depend on the sex of the fetus [ 60 , 64 , 65 ]. In normal pregnancies, maternal microvascular vasodilatation, which is induced by placental corticotrophin-releasing hormone, is greater in pregnant women carrying male fetuses than in those carrying female fetuses.
In pregnancies complicated by pre-eclampsia, microvascular vasodilatation in women carrying a male fetus is weaker than that in normotensive women carrying a male fetus, whereas no such difference is observed in women carrying female fetuses [ 64 ]. The human placenta adapts in a sexually dimorphic manner to chronic maternal asthma. In this situation, female fetal growth is limited, increasing the chances of survival, whereas male fetuses grow normally, this normal growth being associated with a poor outcome in cases of acute asthma exacerbation [ 33 ].
How unbalanced parental nutrition perturbs these differences Placental growth has been shown to respond to maternal influences, including nutrition. There is evidence that the responses are different for the sexes. Studies among babies born around the time of the Dutch famine near the end of the Second World War — have provided insight into the effects of undernutrition on placental size and efficiency in humans, as well as regarding the existence of sex differences in these effects.
Maternal undernutrition in early gestation resulted in a smaller placenta with the decrease in placental area being greater for boys than for girls. Famine also impaired placenta development even for pregnancies occurring after the famine had officially ended. Famine in mid to late gestation made the placenta less efficient as indicated by being born lighter than predicted from placental area, but more efficient when the famine occurred in early gestation or for conceptuses conceived after the famine had ended, since such babies were heavier than predicted [ 20 ].
In addition to the sexual dimorphism in the acute effects of undernutrition on placental size, the association between placental size and later health also appeared to differ between the sexes. In men, the association between placental size and later hypertension was completely reversed by famine exposure, while the associations were unaltered by famine in women [ 14 ].
Consistent with observations in humans, the restriction of placental function alters heart development in sheep fetuses, and small size at birth is associated with more components of metabolic syndrome in adult rams than in adult ewes [ 66 , 67 ].
Experimental and epidemiological studies in humans and animals also demonstrate an association between low or high FPI and impaired glucose tolerance, blood pressure and coronary heart disease [ 68 ]. The size and shape of the placenta are predictive of childhood blood pressure. Changes in the placentation process affecting implantation, the expansion of the chorionic surface in mid-gestation or the compensatory expansion of the chorionic surface in late gestation may affect blood pressure responses and the potential development of hypertension later in life.
The adverse effects of small placental size may be compounded by those of poor maternal nutrition, whereas the area of the placenta may expand to compensate for fetal undernutrition in better-nourished mothers [ 69 ].
Changes in placental structure, activity or physiology may thus contribute to the programming of cardiovascular disease CVD in sex-specific ways [ 22 , 39 , 70 ]. For example hypertension in the male subjects in the Helsinki birth cohort born between and was associated with a long minor diameter of the placenta.
Growth along this minor axis may be more sensitive to nutritional factors than growth along the major axis [ 71 ]. By contrast, hypertension in women was associated with a small placental area at birth, potentially indicating lower levels of nutrient delivery to the fetus. The greater dependence of boys on the diet of their mothers may enable them to make the best use of increases in food supply, but it also leaves them vulnerable to food shortages.
This may be reflected in the tendency of men to have higher blood pressure and to die younger than women [ 72 ]. The effects of maternal undernutrition on placental growth and development have been studied in detail. However, fewer studies have focused on the potentially deleterious effects of maternal overnutrition or metabolic disturbances on the future health of the offspring, particularly as concerns the development of metabolic syndrome or the combination of obesity, type 2 diabetes T2D and CVD [ 53 , 73 ].
The embryo may also react to maternal overnutrition even before the placenta is formed - at the oocyte, zygote or blastocyst stage [ 74 , 75 ]. Moreover there are now convincing data showing that ancestral exposure to an environmental compound modifies the perception and response of the offspring to stress experienced during their own life history.
While the effect of fetal sex on placental development and growth are known, there is relatively little known concerning sex differences in the context of overnutrition. Interestingly expression studies, although rare, do show a sex effect [ 27 , 61 ]. The Aberdeen Maternity and Neonatal Databank involving 55, pregnancies showed that maternal body mass index was positively associated with placental hypertrophy and birth weight but negatively associated with FPI, suggesting that being overweight or obese was associated with greater placental weight but lower placental efficiency [ 45 ].
In humans, placental weight and birth weight are lower in mothers with high carbohydrate intakes in early pregnancy. Low maternal intakes of dairy and meat proteins in late pregnancy are also associated with lower placenta weight and birth weight [ 76 ]. In mice, maternal obesity, T2D and a high-fat diet HFD during gestation increase adiposity and modify metabolism and blood pressure in adult offspring fed a control diet CD , revealing a predisposition to the development of metabolic syndrome [ 77 , 78 ].
These findings suggest that impaired placental development under conditions of maternal overnutrition modifies fetal programming, resulting in impaired responses to diet in adulthood [ 22 , 27 , 71 , 79 , 80 ]. In pregnant mice fed a HFD during gestation, placental weight was higher and placental efficiency FPI lower, regardless of the sex of the fetus, without any gross changes in the areas or proportions of the labyrinth and junctional zone layers [ 81 ]. There have been few studies of paternal non-genetic effects on the health of the offspring in humans.
However, epidemiological studies have suggested that a relationship between maternal grandmother's age and a major autistic trait, or paternal grandfathers access to food and rates of obesity and cardiovascular disease in subsequent generations in a sex-specific manner [ 82 , 83 ]. These aspects have been studied more thoroughly in rodents, in which clear evidence has been obtained for paternal effects on the phenotype and health of the offspring [ 84 ].
In particular paternal fasting before mating [ 85 ], paternal exposure to a HFD [ 8 ] or to a low-protein diet [ 6 ], and maternal caloric undernutrition during late gestation [ 7 ] all have been shown to alter metabolic function in the offspring. Additionally a human study involving singletons found a positive association between paternal weight and placental weight [ 86 ].
Thus, like maternal exposure, prior paternal exposure may have effects on placenta growth. However, to our knowledge, the effects of prior paternal exposure on placenta growth, size and shape have yet to be investigated, in order to elucidate mechanisms by which paternal influences, not just maternal ones, may be transmitted to the embryo, hence to the placenta. Parental stress and behavior, neurobiology Prenatal exposure to maternal stress, depression and pathogenic infections are associated with a higher risk for the development of neurodevelopmental disorders, including schizophrenia and autism [ 13 , 87 ].
Early childhood adversity has also been associated with earlier cancer incidence [ 11 ]. Clear differences between the sexes have been found in the programming of emotionality in the offspring and strategies for coping with stress, with the activational effects of testosterone producing females with male-like strategies in tests of passive coping, but with female-like behavior in tests of active coping [ 46 ].
Animal models of prenatal stress psychological, behavioural, nutritional, or metabolic… have identified major sex- and time-specific effects on the offspring. Maternal stress is associated with the dysregulation of stress pathways, a common feature in most neurodevelopmental disorders. Stress in early pregnancy has a significant sex-dependent effect on placental gene expression, modifying the fetal transport of key growth factors and nutrients [ 88 ].
Synthetic glucocorticoids affect the fetal programming of hypothalamic-pituitary-adrenal axis function and behavior [ 89 ]. Sex-specific differences in the cortisol stress response occur before birth, with much higher levels of cortisol output for male than for female fetuses [ 91 ]. Multigenerational programming in glucocorticoid-programmed rats is associated with effects on fetal and placental weight that are generation-specific and dependent on the parent of origin [ 92 ].
Recent reports have also highlighted the possibility of paternal transmission of stress-induced conditions, such as social defeat [ 93 ] and chronic and unpredictable postnatal maternal separation [ 94 ]. Behavioral adaptations that occur after the stress of chronic social defeat can be transmitted from the father to his male and female F1 progeny.
The male offspring of defeated fathers also display increased baseline plasma levels of corticosterone and decreased levels of vascular endothelial growth factor [ 93 ]. Chronic and unpredictable postnatal maternal separation leads to perturbations in social abilities and serotonergic functions as well as traumatic experiences in early life [ 87 ]. Fetal death has no immediate influence on progesterone production, suggesting that the fetus is a negligible source of substrate.
Enzymes in the placenta cleave the cholesterol side chain, yielding pregnenolone, which in turn is isomerized to progesterone ; to mg of progesterone are produced daily by the third-trimester placenta, and most enters the maternal circulation see Figure 16—2. Whereas exogenous hCG stimulates progesterone production in early pregnancy, hypophysectomy, adrenalectomy, or oophorectomy have no effect on progesterone levels after the luteo-placental shift at 7 to 9 weeks' gestation.
Likewise, the administration of adrenocorticotropin ACTH or cortisol does not influence placental progesterone secretion. Insufficient production of progesterone may contribute to failure of implantation, recurrent pregnancy loss, and preterm delivery. Progesterone , along with relaxin and nitric oxide, maintains uterine quiescence during pregnancy. Progesterone also inhibits T cell—mediated allograft rejection.
Thus, high local concentrations of progesterone may contribute to immunologic tolerance by the uterus of invading trophoblast tissue from the semiallogeneic fetus. Most of the placental estrogens are derived from fetal androgens, primarily dehydroepiandrosterone DHEA sulfate. Fetal DHEA sulfate, produced mainly by the fetal adrenal, is converted by placental sulfatase to free DHEA and then, through enzymatic pathways common to steroid-producing tissues, to androstenedione and testosterone.
These androgens are finally aromatized by the placenta to estrone and estradiol , respectively.
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Gonads and placental hormones in gestational diabetes csgo guru betting advice nfl
Risk Factors for Gestational Diabetes
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Your pancreas works hard to create insulin when you have gestational diabetes, but the insulin has little effect on your blood glucose levels. Thus, more blood glucose passes through the placenta, resulting in elevated blood glucose levels in the infant. Hormone of human chorionic gonadotropin hCG. This hormone is produced only during pregnancy. Human placental lactogen hPL. This hormone is sometimes referred to as chorionic human somatomammotropin.
This set of hormones aids in the development of female sexual characteristics. Does the anterior placenta enhance the risk of developing gestational diabetes? An increased risk of pregnancy-induced hypertension, gestational diabetes, placental abruption, intrauterine growth retardation, and intrauterine foetal mortality is related with anterior placental implantation. What four hormones does the placenta secrete? This hormone is generated nearly entirely in the placenta during pregnancy.
Can hCG induce pregnancy-related diabetes? Higher hCG levels in early pregnancy are connected with a reduced risk of gestational diabetes. Maternal fT4 may serve as a crucial mediator in this relationship. How can I determine whether my placenta has gestational diabetes?
A abrupt decrease in blood sugar levels — levels decreasing significantly lower than normal to extremely low levels 2. Consult a medical expert if you observe a decline of this magnitude. Does stress induce gestational diabetes? Women with gestational diabetes mellitus GDM have more psychological stress than other pregnant women.
As the study of prenatal diabetes mellitus has progressed, research has shown that anxiety and depression are also significant causes of gestational diabetes mellitus. How can I reduce my chance of developing gestational diabetes?
Increase your consumption of lean proteins, such as fish and tofu, to feel filled for longer. Eat an abundance of veggies and whole grains to increase your fiber consumption. Which of the following may raise the risk of gestational diabetes in women?
Although any pregnant woman may acquire gestational diabetes, the following variables may raise her risk: Obesity or morbid obesity. A history of diabetes in the family Having previously delivered a baby weighing more than 9 pounds. Can excessive sugar intake lead to gestational diabetes? A: Consuming sugary meals does not raise the likelihood of developing gestational diabetes. If you are diagnosed with gestational diabetes, you will need to control your carbohydrate consumption in order to maintain optimal blood sugar levels.
This would involve limiting your sugar consumption. Does elevated progesterone lead to diabetes? In addition, a recent meta-analysis revealed that supplementation with OH progesterone caproate was associated with an increased risk of gestational diabetes At what week does gestational diabetes develop? Gestational diabetes typically develops between the 24th and 28th week of pregnancy, thus you will likely be tested between the 24th and 28th week.
If you are at at risk for gestational diabetes, your physician may test you early. Will progesterone boost blood sugar? What role does an endocrinologist play in the treatment of gestational diabetes? Your endocrinologist will evaluate the impact of diabetes on you and provide you with guidance on how to manage gestational diabetes. The placenta supplies a growing fetus with nutrients and produces a variety of hormones to maintain the pregnancy.
Some of these hormones, such as human placental lactogen, have a blocking effect on insulin that usually begins 20 to 24 weeks into the pregnancy. The contra-insulin effect of placental hormones leads to higher levels of maternal blood glucose after eating post-prandial levels that may aid fetal growth. Normally, the mother's beta cells can produce additional insulin to overcome the insulin resistance of pregnancy. As the placenta grows, more hormones are produced, and insulin resistance becomes greater.
When the mother's production of insulin is not enough to overcome the effect of the placental hormones, gestational diabetes mellitus GDM results. GDM is defined as "carbohydrate intolerance of varying degrees of severity with onset or first recognition during pregnancy" 1. The main complications of GDM are increased fetal size, which may complicate delivery, and hypoglycemia in the baby immediately after delivery. Women with GDM generally have normal blood sugar levels during the critical first trimester before the 13th week of pregnancy.
This is in contrast to patients with type 1 diabetes, where hyperglycemia in this period may cause congenital birth defects. After a positive screening test, the diagnosis of GDM is made by a glucose tolerance test. In this test, a sugary drink is given, and a series of blood tests are taken at set time intervals Table 1.
If hyperglycemia is detected, treatment begins with a change in diet and an increase in exercise. If these lifestyle changes fail to control blood glucose levels, insulin therapy is started.
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