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Sometimes a woman with gestational diabetes must also take insulin. Besides causing discomfort to the woman during the last few months of pregnancy, an extra-large baby can lead to problems during delivery for both the mother and the baby. The mother might need a C-Section to deliver the baby. The baby can be born with nerve damage due to pressure on the shoulder during delivery.

A woman who has diabetes that is not well controlled has a higher chance of needing a C-section to deliver the baby. When the baby is delivered by a C-section, it takes longer for the woman to recover from childbirth. It is a serious problem that needs to be watched closely and managed by her doctor.

High blood pressure can cause harm to both the woman and her unborn baby. It might lead to the baby being born early and also could cause seizures or a stroke a blood clot or a bleed in the brain that can lead to brain damage in the woman during labor and delivery. Women with diabetes have high blood pressure more often than women without diabetes. Listen to this Podcast: Gestational Diabetes Low Blood Sugar Hypoglycemia People with diabetes who take insulin or other diabetes medications can develop blood sugar that is too low.

Low blood sugar can be very serious, and even fatal, if not treated quickly. Seriously low blood sugar can be avoided if women watch their blood sugar closely and treat low blood sugar early. A dietitian can help you create a healthy meal plan.

Learn more about diabetes meal planning. A dietitian can also help you learn how to control your blood sugar while you are pregnant. To find a registered dietician near you, please visit The Academy of Nutrition and Dietetics website. Exercise Regularly Exercise is another way to keep blood sugar under control.

This is accomplished by upregulating the placental transferrin receptor, although more pronounced receptor glycosylation associated with hyperglycemia may reduce its affinity for transferrin binding 34 — A direct effect of fetal oxygen on placental vascular function cannot be ruled out, but remains to be demonstrated. Collectively, the fetoplacental unit adapts structurally and functionally to facilitate oxygen delivery to the fetus in normal pregnancy and beyond in situations of metabolically induced enhanced oxygen demand.

These changes result in a shorter overall oxygen diffusive conductance 37 , Preventing Impairment of Fetoplacental Blood Flow—Avoiding Preatherosclerotic Lesions Another example of placental responses aiming to protect fetal development can be found in the mechanisms preventing preatherosclerotic lesions in the fetoplacental circulation. On the maternal side, atheromas in spiral arteries have been found and are more frequent in T1D Foam cells can form in the intervillous space in situations of maternal hypercholesterolemia 40 , and in the fetal aorta, fatty streaks can be formed However, no similar lesions have been identified yet in the fetoplacental circulation.

This suggests that highly efficient mechanisms for cholesterol efflux from placental vessels must be in place. Indeed, we have identified cholesterol efflux transporters ABCA1 and ABCG1 on fetoplacental endothelial cells and have delineated a two-step mechanism for the endothelial cells to efflux cholesterol Fetal HDL2 will then be taken up by the liver. This represents an efficient mechanism for fetoplacental endothelial cells to shuttle their cholesterol to the fetal liver, thus protecting against formation of preatherosclerotic lesions in the vasculature of the placenta proper.

In GDM, placental endothelial cells synthesize more cholesterol because of upregulation of HMG-CoA reductase, the rate-limiting enzyme in the cholesterol biosynthetic pathway. Yet total cholesterol content in the endothelium is unaffected by GDM, because cholesterol efflux mechanisms are upregulated by oxysterols in the fetal circulation, which form de novo from cholesterol through reactive oxygen species—induced oxidation Fetal insulin is one of the regulators of PLTP activity Thus, in GDM, all mechanisms that ensure cholesterol homeostasis at the fetoplacental interface are upregulated to avoid vascular damage and compromised blood flow due to the formation of preatherosclerotic lesions.

The mechanisms related to cholesterol homeostasis are further supported by a reduction of both forms of intercellular adhesion molecule 1 ICAM-1 —the surface bound and the soluble form—on placental endothelial cells. Their levels are in an inverse relationship with maternal BMI. These proteins are markers of vascular inflammation The low ICAM-1 protein levels in GDM can be regarded as an additional protective mechanism to avoid transmigration of fetal leukocytes into the subendothelial space of the fetoplacental circulation, thereby also contributing to reducing the risk of preatherosclerotic lesions.

In both examples above, the fetus provides the signals inducing the cellular and molecular mechanisms that facilitate placental adaptation Fig. This represents a change in paradigm: previously, maternal control of placental development and function was presumed; the findings discussed above establish the importance of fetoplacental signaling. On the basis of the developmental shift of the insulin receptor location from the surface facing the maternal circulation to that facing the fetal circulation, we have previously proposed that maternal factors govern placental development and function mostly early in pregnancy, whereas the fetus gradually takes over control of its own organ in later stages of pregnancy Figure 3 View large Download slide Placental adaptation for fetal protection.

Fetal signals induce placental structural and functional adaptation as protective measures. Insulin is one of the drivers of the proangiogenic response to low oxygen levels, to which in turn fetal insulin contributes by stimulating metabolism.

Insulin also upregulates PLTP, which facilitates removal of excessive cholesterol released from the placental endothelium. Glucose, through reactive oxygen species, leads to formation of oxysterols, which induce cholesterol efflux transporters. Cooperation of these mechanisms ensures that cholesterol content in the endothelium is unaltered in GDM despite enhanced cholesterol synthesis and that the cholesterol released into the fetal circulation is removed by the fetal liver. Close modal Modifiers of Placental Adaptation The processes described above are just examples of how the placenta protects the fetus at the end of pregnancy and, in doing so, acts as a friend for the fetus.

However, these examples of placental changes to maintain a stable fetoplacental interaction through homeostatic mechanisms have been established under certain experimental conditions, and generalization is difficult at this point. There are some aspects that may modify the protective function or at least shift the level of tolerance toward metabolic and inflammatory disturbance.

If maternal disturbances affect fetal growth and development, this depends not only on the placental homeostatic capacity, but also on the metabolic load to which the fetoplacental unit is exposed Fig. Figure 4 View large Download slide Homeostatic capacity vs. The placental homeostatic capacity allows adaptations to fetal needs. In this situation, the placenta serves as a friend to the fetus. However, with increasing metabolic load, i. The placenta would then be the foe of the fetus.

Close modal Effects of Fetal Sex The placenta is well known to show sex-specific differences in expression of genes and function, and the nature of these differences depends on placental cell type 48 — Also, the response to environmental stimuli, such as maternal dietary factors, differs between sexes This seems to favor flexibility and adaptive responses in placentas of female fetuses. Insulin resistance found in female neonates born to women with diabetes serves as a cellular antioxidant defense mechanism 52 and is a further protective strategy of the fetoplacental unit designed by evolution to favor reproductive outcome in females.

The association of cord blood insulin with subcutaneous fat in the newborn is sex specific The presence of transcriptome sex differences in the late first trimester placenta suggests different susceptibility and stress response mechanisms early on The protective mechanisms described above were all established with endothelial cells from female fetoplacental units, and it remains to be seen whether they are also operative to a similar extent in male endothelial cells.

Heterogeneity of the Placenta While it is obvious that distinct placental cell types respond differently to environmental cues, even within distinct placental cell types, regional differences in the protein repertoire may lead to different responses even within distinct cell types.

A clear example of such regional differences is the presence and density of endothelial insulin receptors along the vascular tree 55 , with high density in areas destined to drive vascular growth. Thus, the response to fetal hyperinsulinemia likely differs by region. Currently, it is unclear whether regions with low receptor density show similar responses as described previously. It can be hypothesized that regional differences are also present for all other cell-surface or intracellular molecules.

Hence, functional responses of the placenta to changes in utero and the fetoplacental circulation may vary by region. For example, proteomic analyses of placentas in well-controlled GDM at the end of pregnancy demonstrated only minor changes, although some proteins were hyperglycosylated 56 , Placental lipid metabolism is strikingly and nonlinearly affected by maternal conditions.

The enzyme endothelial lipase 58 is the predominant lipase on the microvillous membrane of the syncytiotrophoblast. It is involved in hydrolyzing phospholipids and triglycerides, and the fatty acids released by lipolysis can be taken up by the syncytiotrophoblast for further metabolism. The enzyme responds only when threshold levels are exceeded, again demonstrating a protective effect for the fetoplacental unit. The free fatty acids taken up by the placenta enter metabolic pathways, one of which is their re-esterification and storage as triglycerides in syncytiotrophoblast lipid droplets 59 , The removal of free fatty acids from the cytoplasm protects the syncytiotrophoblast from lipotoxicity 61 and, hence, can be regarded as a further protective mechanism.

In mothers with modest obesity obesity class I , the placental triglyceride content is higher than in lean women. However, more pronounced maternal obesity obesity classes II and III is not associated with a further increase in placental triglyceride content, which levels off, demonstrating the capacity limit of protection. It is unknown whether the excess fatty acids in the syncytiotrophoblast not stored in triglycerides affect trophoblast function or spill over to the fetal circulation and contribute to fetal fat accretion.

Conclusions and Future Prospects In this article, I have attempted to bring together the available evidence and embed it in a conceptual framework encompassing early and late pregnancy periods. Despite manifold studies, there is no evidence for a placental role late in pregnancy contributing to adverse outcomes. However, these studies including our own have the major limitation that 1 only mild forms of maternal metabolic, endocrine, and inflammatory disturbance have been included and 2 they have focused exclusively on the end of pregnancy.

In other situations, placental response may be different. Hence, the answer to my question raised at the outset of this article, of the placenta being a friend or foe for the fetus, is not straightforward but rather more complex. The scarce information about effects of the diabetic or obese environment on the placenta early in pregnancy does not yet allow a conceptual conclusion. This pregnancy period is an underresearched area because of ethical constraints.

Animal studies do not help because animals follow different growth strategies than humans and their placentas are structurally and functionally different. In vitro studies need to take into account the changes in ambient oxygen tension during the first trimester as well as the week of pregnancy when the placental tissue was collected for research.

Clinical research can strongly contribute by measuring crown-rump length as well as placental volume from as early as possible in the first trimester and by correlating both measures with maternal metabolic and endocrine factors. This would allow determination of the effects of early metabolic changes on placental and fetal growth throughout pregnancy as well as on neonatal outcomes, including body composition. Much more research is needed in more severe metabolic, endocrine, and inflammatory conditions of the mother at the end of gestation.

The continuous improvement in maternal metabolic control has made it difficult to prospectively carry out these studies. Analyzing archival material with state-of-the-art methods developed especially for these types of samples may be an option.