Abstract:The effect of diabetic metabolism on the human vascular wall studied, using the fetal cardiovascular system at birth as an experimental model. The ultrastructure of umbilical arteries from nine newborn children of nonsmoking diabetic mothers (White group D) was compared with that of 30 healthy nonsmokers. Intimal cushions, thickening of the basement membrane often with a multilaminal appearance, and glycogen accumulations, both in the cells of the intima and the media, were found. The cells of the intima were … Show more
“…However, a slight, but non-significant increase in the inflammatory cells (lymphocytes) was found on the surface of umbilical venous endothelium in diabetic pregnancies. This is in line with previous findings of the injured endothelium in umbilical arteries in diabetic pregnancies: endothelial cell death and formation of a thick intima layer with myoendothelial cells, intimal cushions and loose junctions [12,24]. On the other hand, inflammatory cells may be the first signs of hyperglycaemia-induced endothelial injury due to increased oxidative stress [43] and reactive oxygen species [25] seen in fetoplacental vascular dysfunction in diabetic pregnancies.…”
Section: Infants Born To Diabetic Motherssupporting
confidence: 91%
“…The umbilical cord cells possess a wide differentiation potential and plasticity while being exposed to various pregnancy-induced changes [11], and in accordance, the ultrastructure of human umbilical arteries is altered in diabetic pregnancies [12,13]. Further, the umbilical vein endothelial cells from diabetic pregnancies show increased gene expression and activity of endothelial nitric oxide synthase, indicating altered vascular reactivity [14].…”
Section: Introductionmentioning
confidence: 80%
“…This pathway was downregulated with 15 genes including extracellular matrix regulating genes degrading the basement membrane (MMP2), cytokines and growth factors regulating vascular stability (COL8A, MEF2C), and signal transduction genes (NOTCH4, NPPB, EDN1, Semaphorin 5A, Thrombospondin 2, T-box 1, SRY-box 17, Cadherin 2, Protein tyrosine phosphatase receptor B, CD34, Angiotensinogen, Glutamyl aminopeptidase) coding functions that are generally known to be linked to insufficient angiogenesis in diabetes [21]. Previously, diabetic pregnancies have been associated with ruptured collagen fibers and oedema, basement membrane arterial thickening, intimal cushions with glycogen accumulation, rupture of the endothelial lining of the arteries and dilated veins with smooth muscle fiber fragmentation in umbilical cords [12,23,24]. In this study, we found thicker venous muscle walls and increased intimamedia areas in the umbilical veins and arteries of neonates born to diabetic mothers.…”
“…However, a slight, but non-significant increase in the inflammatory cells (lymphocytes) was found on the surface of umbilical venous endothelium in diabetic pregnancies. This is in line with previous findings of the injured endothelium in umbilical arteries in diabetic pregnancies: endothelial cell death and formation of a thick intima layer with myoendothelial cells, intimal cushions and loose junctions [12,24]. On the other hand, inflammatory cells may be the first signs of hyperglycaemia-induced endothelial injury due to increased oxidative stress [43] and reactive oxygen species [25] seen in fetoplacental vascular dysfunction in diabetic pregnancies.…”
Section: Infants Born To Diabetic Motherssupporting
confidence: 91%
“…The umbilical cord cells possess a wide differentiation potential and plasticity while being exposed to various pregnancy-induced changes [11], and in accordance, the ultrastructure of human umbilical arteries is altered in diabetic pregnancies [12,13]. Further, the umbilical vein endothelial cells from diabetic pregnancies show increased gene expression and activity of endothelial nitric oxide synthase, indicating altered vascular reactivity [14].…”
Section: Introductionmentioning
confidence: 80%
“…This pathway was downregulated with 15 genes including extracellular matrix regulating genes degrading the basement membrane (MMP2), cytokines and growth factors regulating vascular stability (COL8A, MEF2C), and signal transduction genes (NOTCH4, NPPB, EDN1, Semaphorin 5A, Thrombospondin 2, T-box 1, SRY-box 17, Cadherin 2, Protein tyrosine phosphatase receptor B, CD34, Angiotensinogen, Glutamyl aminopeptidase) coding functions that are generally known to be linked to insufficient angiogenesis in diabetes [21]. Previously, diabetic pregnancies have been associated with ruptured collagen fibers and oedema, basement membrane arterial thickening, intimal cushions with glycogen accumulation, rupture of the endothelial lining of the arteries and dilated veins with smooth muscle fiber fragmentation in umbilical cords [12,23,24]. In this study, we found thicker venous muscle walls and increased intimamedia areas in the umbilical veins and arteries of neonates born to diabetic mothers.…”
“…In an electron-microscopic study, Asmussen [18] showed intimal cushions, thickening of basement membrane, often with a multilaminal appearance, and glycogen accumulations, both in the cells of the umbilical artery intima, and media of infants of nonsmoking, white group D diabetic mothers, but the correlation of these findings with clinical and laboratory data was not investigated. In order to prove the hypothesis that preclinical atherosclerosis begins in utero, we measured uIMT, puWT and ruWT by radiological and pathological techniques.…”
Background: Large for gestational age (LAG) neonates who had been exposed to an intrauterine environment of either diabetes or maternal obesity are at increased risk of developing the metabolic syndrome. This can be explained by exposure to high glucose and insulin levels in utero which alter fetal adaptation and programming. Objectives: The aim of the study was to evaluate the onset of preclinical atherosclerosis in utero. Methods: We measured umbilical artery wall thickness (ruWT) in the third trimester by obstetric ultrasound and umbilical artery intima-media thickness (uIMT) in pathologic specimens of umbilical cords obtained shortly after delivery and investigated the relation between these measurements and serum insulin level and C-peptide level in cord blood and assessed insulin resistance with the homeostasis model assessment of insulin resistance (HOMA-IR) in infants of diabetic mothers (IDMs), i.e. the study group, which was divided into a large for gestational age group (LGA)-IDM group and an appropriate for gestational age group (AGA)-IDM group and compared with a control group. Results: The LGA-IDM group had significantly higher insulin (p < 0.001), C-peptide (p = 0.018) and HOMA-IR levels (p < 0.001) compared with the AGA-IDM and control groups. The LGA-IDM group had significantly larger ruWT (p = 0.013) and uIMT (p < 0.001) compared with the AGA-IDM and the control groups. The LGA-IDM group had increased uIMT and ruWT that correlated with the severity of maternal hyperglycemia. Conclusions: Measurement of ruWT in the third trimester is feasible, reproducible and strongly correlated with pathological serum insulin, C-peptide in cord blood and HOMA-IR levels.
“…It is usually patent for some time after birth and may be used for exchange transfusions during early infancy [Moore, 1980]. Electron microscope studies of umbilical vasculature have focused mainly on intimal features occurring in normal and pathological cases, which arc present at birth [Asmussen, 1980;Las Heras and Haust, 1981], However, detailed electron miscroscopic developmental studies of umbilical vasculature from midgestation through early postnatal life have not been reported. In this study, the differences in cell fea tures between umbilical arteries and veins at different stages of developmental are evaluated, with special emphasis on lipid droplet formation.…”
Qualitative and quantitative changes in the human umbilical artery and vein were observed in 15 human specimens at different stages of development. Features such as intimal thickening and cellular lipid accumulation were found in umbilical vasculature. Cellular origin and quantification of lipid-containing cells were determined by electron microscopy. Within 1 month after birth, lipid-containing cells originating from macrophages were observed in the umbilical artery, while those originating from smooth muscle cells were observed in both the umbilical artery and vein. Lipid droplet formation appeared to be independent and different in macrophages and smooth muscle cells; the former cells were stimulated to produce lipid droplets primarily by plasma insudation and the latter cells primarily by hypoxia. These findings indicate that ultrastructural changes observed in closing umbilical vasculature may closely parallel and serve as a model for atherosclerotic changes which occur in mature vessels.
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