Erratum to: 4 INFLUENCE OF A MATERNAL DIABETES MELLITUS TYPE 1 ON LIPID AND CHOLESTEROL METABOLISM IN RABBIT PRE-IMPLANTATION EMBRYOS

2013 ◽  
Vol 25 (1) ◽  
pp. 149
Author(s):  
M. Schindler ◽  
M. Pendzialek ◽  
T. Plösch ◽  
J. M. Knelangen ◽  
J. Gürke ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Embryo Development ◽  
Maternal Diabetes ◽  
Early Embryo ◽  
Cholesterol Concentration ◽  
Early Embryo Development ◽  
Diabetic Rabbits ◽  
Maternal Diabetes Mellitus

The incidence of overweight and obesity has reached epidemic levels worldwide. Even more alarming is the increasing prevalence of metabolic diseases in younger children and adolescents. The rate of women with diabetes mellitus in child-bearing age is rising, too. According to the developmental origins of health and disease (DOHaD) paradigm, exposure to a hyperglycaemic environment in utero may programme physiology and metabolism permanently, with long-term consequences for offspring health. Experimental evidence indicates that programming of obesity does occur during early embryo development, a period where many women are unaware of pregnancy. To study effects of maternal diabetes mellitus on early embryo development, we induced a type I diabetes through alloxan treatment of female rabbits. In diabetic rabbits, the triglyceride and cholesterol concentrations were altered in serum and the cholesterol concentration in the uterine secretions was elevated. Lipid content of 6-day-old blastocysts was analysed after Oil Red staining and whole mount histochemistry or with Nile Red by fluorescence-activated cell sorting (FACS). Analysis by FACS revealed an approximately 2-fold increase in lipid droplets in blastocysts grown under diabetic conditions. The expression of genes important for lipid metabolism, such as fatty acid transport protein 4 (FATP4), fatty acid-binding protein 4 (FABP4), carnitine palmitoyltransferase 1 (CPT-1), and lipoprotein lipase (LPL), were determined by real-time PCR and showed distinct differences between diabetic and control blastocysts. Immunohistochemical staining of FABP4 was clearly increased in blastocysts grown under diabetic conditions and showed a cell lineage-specific distribution. Two transcription factors, peroxisome proliferator-activated receptor α (PPARα) and PPARγ, with key functions in lipid metabolism and adipogenic differentiation, were increased in blastocysts from diabetic rabbits. We show that maternal diabetes mellitus leads to alteration in lipid metabolism and to triglyceride accumulation in blastocysts. Its long-lasting consequences (e.g. for adipose cell differentiation) need attention and further investigation.

scholarly journals Erratum to: 4 INFLUENCE OF A MATERNAL DIABETES MELLITUS TYPE 1 ON LIPID AND CHOLESTEROL METABOLISM IN RABBIT PRE-IMPLANTATION EMBRYOS

2013 ◽  
Vol 25 (3) ◽  
pp. 587
Author(s):  
M. Schindler ◽  
M. Pendzialek ◽  
T. Plösch ◽  
J. M. Knelangen ◽  
J. Gürke ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Embryo Development ◽  
Maternal Diabetes ◽  
Early Embryo ◽  
Cholesterol Concentration ◽  
Early Embryo Development ◽  
Diabetic Rabbits ◽  
Maternal Diabetes Mellitus

The incidence of overweight and obesity has reached epidemic levels worldwide. Even more alarming is the increasing prevalence of metabolic diseases in younger children and adolescents. The rate of women with diabetes mellitus in child-bearing age is rising, too. According to the developmental origins of health and disease (DOHaD) paradigm, exposure to a hyperglycaemic environment in utero may programme physiology and metabolism permanently, with long-term consequences for offspring health. Experimental evidence indicates that programming of obesity does occur during early embryo development, a period where many women are unaware of pregnancy. To study effects of maternal diabetes mellitus on early embryo development, we induced a type I diabetes through alloxan treatment of female rabbits. In diabetic rabbits, the triglyceride and cholesterol concentrations were altered in serum and the cholesterol concentration in the uterine secretions was elevated. Lipid content of 6-day-old blastocysts was analysed after Oil Red staining and whole mount histochemistry or with Nile Red by fluorescence-activated cell sorting (FACS). Analysis by FACS revealed an approximately 2-fold increase in lipid droplets in blastocysts grown under diabetic conditions. The expression of genes important for lipid metabolism, such as fatty acid transport protein 4 (FATP4), fatty acid-binding protein 4 (FABP4), carnitine palmitoyltransferase 1 (CPT-1), and lipoprotein lipase (LPL), were determined by real-time PCR and showed distinct differences between diabetic and control blastocysts. Immunohistochemical staining of FABP4 was clearly increased in blastocysts grown under diabetic conditions and showed a cell lineage-specific distribution. Two transcription factors, peroxisome proliferator-activated receptor α (PPARα) and PPARγ, with key functions in lipid metabolism and adipogenic differentiation, were increased in blastocysts from diabetic rabbits. We show that maternal diabetes mellitus leads to alteration in lipid metabolism and to triglyceride accumulation in blastocysts. Its long-lasting consequences (e.g. for adipose cell differentiation) need attention and further investigation.

scholarly journals Embryonic fatty acid metabolism in diabetic pregnancy: the difference between embryoblasts and trophoblasts

2020 ◽  
Vol 26 (11) ◽  
pp. 837-849
Author(s):  
Maria Schindler ◽  
Dirk Dannenberger ◽  
Gerd Nuernberg ◽  
Mareike Pendzialek ◽  
Katarzyna Grybel ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Saturated Fatty Acids ◽  
Maternal Diabetes ◽  
Maternal Blood ◽  
Maternal Plasma ◽  
Metabolic Adaptation ◽  
Diabetic Rabbits ◽  
Maternal Diabetes Mellitus

Abstract During the first days of development the preimplantation embryo is supplied with nutrients from the surrounding milieu. Maternal diabetes mellitus affects the uterine microenvironment, leading to a metabolic adaptation processes in the embryo. We analysed embryonic fatty acid (FA) profiles and expression of processing genes in rabbit blastocysts, separately in embryoblasts (EBs) and trophoblasts (TBs), to determine the potential consequences of maternal diabetes mellitus on intracellular FA metabolism. Insulin-dependent diabetes was induced by alloxan in female rabbits. On Day 6 post coitum, FA profiles in blastocysts (EB, TB and blastocoel fluid) and maternal blood were analysed by gas chromatography. The expression levels of molecules involved in FA elongation (fatty acid elongases, ELOVLs) and desaturation (fatty acid desaturases, FADSs) were measured in EB and TB. Maternal diabetes mellitus influenced the FA profile in maternal plasma and blastocysts. Independent from metabolic changes, rabbit blastocysts contained a higher level of saturated fatty acids (SFAs) and a lower level of polyunsaturated fatty acids (PUFAs) compared to the FA profile of the maternal plasma. Furthermore, the FA profile was altered in the EB and TB, differently. While SFAs (palmitic and stearic acid) were elevated in EB of diabetic rabbits, PUFAs, such as docosahexaenoic acid, were decreased. In contrast, in the TB, lower levels of SFAs and higher levels of oleic acid were observed. EB and TB specific alterations in gene expression were found for ELOVLs and FADSs, key enzymes for FA elongation and desaturation. In conclusion, maternal diabetes mellitus alters embryonic FA metabolism differently in EB and TB, indicating a lineage-specific metabolic adaptive response.

scholarly journals Metabolic Profiling in Blastocoel Fluid and Blood Plasma of Diabetic Rabbits

2020 ◽  
Vol 21 (3) ◽  
pp. 919 ◽  
Author(s):  
Maria Schindler ◽  
Sophia Mareike Pendzialek ◽  
Katarzyna Grybel ◽  
Tom Seeling ◽  
Anne Navarrete Santos
Keyword(s):  
Diabetes Mellitus ◽  
Blood Plasma ◽  
Embryo Development ◽  
Maternal Diabetes ◽  
Diabetic Group ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Maternal Metabolism ◽  
Insulin Dependent ◽  
Maternal Diabetes Mellitus

Metabolic disorders of the mother adversely affect early embryo development, causing changes in maternal metabolism and consequent alterations in the embryo environment in the uterus. The goal of this study was to analyse the biochemical profiles of embryonic fluids and blood plasma of rabbits with and without insulin-dependent diabetes mellitus (DT1), to identify metabolic changes associated with maternal diabetes mellitus in early pregnancy. Insulin-dependent diabetes was induced by alloxan treatment in female rabbits 10 days before mating. On day 6 post-coitum, plasma and blastocoel fluid (BF) were analysed by ultrahigh performance liquid chromatography-tandem mass spectroscopy (UPLC-MS/MS) (Metabolon Inc. Durham, NC, USA). Metabolic datasets comprised a total of 284 and 597 compounds of known identity in BF and plasma, respectively. Diabetes mellitus had profound effects on maternal and embryonic metabolic profiles, with almost half of the metabolites changed. As predicted, we observed an increase in glucose and a decrease in 1,5-anhydroglucitol in diabetic plasma samples. In plasma, fructose, mannose, and sorbitol were elevated in the diabetic group, which may be a way of dealing with excess glucose. In BF, metabolites of the pentose metabolism were especially increased, indicating the need for ribose-based compounds relevant to DNA and RNA metabolism at this very early stage of embryo development. Other changes were more consistent between BF and plasma. Both displayed elevated acylcarnitines, body3-hydroxybutyrate, and multiple compounds within the branched chain amino acid metabolism pathway, suggesting that lipid beta-oxidation is occurring at elevated levels in the diabetic group. This study demonstrates that maternal and embryonic metabolism are closely related. Maternal diabetes mellitus profoundly alters the metabolic profile of the preimplantation embryo with changes in all subclasses of metabolites.

scholarly journals Effects of streptozotocin- and alloxan-induced diabetes mellitus on mouse follicular and early embryo development

Reproduction ◽  
1989 ◽  
Vol 86 (1) ◽  
pp. 1-10 ◽  
Author(s):  
M. P. Diamond ◽  
K. H. Moley ◽  
A. Pellicer ◽  
W. K. Vaughn ◽  
A. H. DeCherney
Keyword(s):  
Diabetes Mellitus ◽  
Embryo Development ◽  
Early Embryo ◽  
Early Embryo Development

Importance of lipid metabolism on oocyte maturation and early embryo development: Can we apply what we know to buffalo?

2019 ◽  
Vol 211 ◽  
pp. 106220
Author(s):  
Diego Fernando Dubeibe Marin ◽  
Nathalia Nogueira da Costa ◽  
Priscilla di Paula Bessa Santana ◽  
Eduardo Baia de Souza ◽  
Otavio Mitio Ohashi
Keyword(s):  
Lipid Metabolism ◽  
Embryo Development ◽  
Oocyte Maturation ◽  
Early Embryo ◽  
Early Embryo Development

Minor Splicing Factors Zrsr1 and Zrsr2 Essential for Gametogenesis, Early Embryo Development and Conversion of Stem Cells into 2C-Like

2019 ◽  
Author(s):  
Isabel Gómez-Redondo ◽  
Priscila Ramos-Ibeas ◽  
Eva Pericuesta ◽  
Benjamín Planells ◽  
Raul Fernández-González ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryo Development ◽  
Early Embryo ◽  
Splicing Factors ◽  
Early Embryo Development

scholarly journals 288 Assessing in vivo placental function in pregnancies complicated by maternal diabetes mellitus

2021 ◽  
Vol 224 (2) ◽  
pp. S188-S189
Author(s):  
Stacey Gold ◽  
Catherine Lopez ◽  
Jessica L. Quistorff ◽  
Sarah Downs ◽  
Sara Iqbal ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Maternal Diabetes ◽  
Placental Function ◽  
Maternal Diabetes Mellitus

scholarly journals LIN28 coordinately promotes nucleolar/ribosomal functions and represses the 2C-like transcriptional program in pluripotent stem cells

2021 ◽  
Author(s):  
Zhen Sun ◽  
Hua Yu ◽  
Jing Zhao ◽  
Tianyu Tan ◽  
Hongru Pan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryo Development ◽  
Pluripotent Stem Cells ◽  
Rna Binding ◽  
Stem Cell Differentiation ◽  
Early Embryo ◽  
Transcriptional Program ◽  
Cell Stage ◽  
Early Embryo Development ◽  
Nucleolar Stress

AbstractLIN28 is an RNA binding protein with important roles in early embryo development, stem cell differentiation/reprogramming, tumorigenesis and metabolism. Previous studies have focused mainly on its role in the cytosol where it interacts with Let-7 microRNA precursors or mRNAs, and few have addressed LIN28’s role within the nucleus. Here, we show that LIN28 displays dynamic temporal and spatial expression during murine embryo development. Maternal LIN28 expression drops upon exit from the 2-cell stage, and zygotic LIN28 protein is induced at the forming nucleolus during 4-cell to blastocyst stage development, to become dominantly expressed in the cytosol after implantation. In cultured pluripotent stem cells (PSCs), loss of LIN28 led to nucleolar stress and activation of a 2-cell/4-cell-like transcriptional program characterized by the expression of endogenous retrovirus genes. Mechanistically, LIN28 binds to small nucleolar RNAs and rRNA to maintain nucleolar integrity, and its loss leads to nucleolar phase separation defects, ribosomal stress and activation of P53 which in turn binds to and activates 2C transcription factor Dux. LIN28 also resides in a complex containing the nucleolar factor Nucleolin (NCL) and the transcriptional repressor TRIM28, and LIN28 loss leads to reduced occupancy of the NCL/TRIM28 complex on the Dux and rDNA loci, and thus de-repressed Dux and reduced rRNA expression. Lin28 knockout cells with nucleolar stress are more likely to assume a slowly cycling, translationally inert and anabolically inactive state, which is a part of previously unappreciated 2C-like transcriptional program. These findings elucidate novel roles for nucleolar LIN28 in PSCs, and a new mechanism linking 2C program and nucleolar functions in PSCs and early embryo development.

Placental Accumulation of Triacylglycerols in Gestational Diabetes Mellitus and Its Association with Altered Fetal Growth are Related to the Differential Expressions of Proteins of Lipid Metabolism

2020 ◽  
Author(s):  
Manoharan Balachandiran ◽  
Zachariah Bobby ◽  
Gowri Dorairajan ◽  
Sajini Elizabeth Jacob ◽  
Victorraj Gladwin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fetal Growth ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Acid Oxidation ◽  
Placental Proteins

Abstract Introduction Gestational diabetes mellitus (GDM) exhibit altered placental lipid metabolism. The molecular basis of this altered metabolism is not clear. Altered placental expression of proteins of lipogenesis and fatty acid oxidation may be involved in the placental accumulation of triacylglycerols (TG). The present study was aimed at investigating the differential expressions of placental proteins related to lipid metabolism among GDM women in comparison with control pregnant women (CPW) and to correlate them with maternal and fetal lipid parameters as well as altered fetal growth. Materials and Methods Maternal blood, cord blood, and placental samples were collected from GDM and CPW. The biochemical parameters, glucose, lipid profile and free fatty acids (FFA) were measured. The placental TG content was measured. Differential placental expressions of proteins; phosphatidylinositol-3-kinase (PI3K) p85α, PI3K p110α,liver X receptor alpha (LXRα), sterol regulatory element binding protein1(SREBP1), fatty acid synthase (FAS), stearyl CoA desaturase1 (SCD1), lipoprotein lipase (LPL),Peroxisome proliferator-activated receptor (PPAR)α and PPARγ were analysed by western blotting and immunohistochemistry. Results Placental protein expressions of PI3K p110α, LXRα, FAS, SCD1, and LPL were found to be significantly higher, whereas PPARα and PPARγ were lower in GDM women compared with CPW. The placental TG content and cord plasma FFA were increased in GDM women compared with CPW. The placental TG content positively correlated with Ponderal index of GDM new-borns. Conclusion Differential expressions of placental proteins related to lipid metabolism in GDM might have led to placental TG accumulation. This might have contributed to the fetal overgrowth in GDM.

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