Polyamines protect rat embryo <i>in vitro</i> from high glucose‐induced developmental delay and dysmorphogenesis

Chirino-Galindo, Gladys; Baiza-Gutman, Luís Arturo; Barrera-Escorcia, Eduardo; Palomar-Morales, Martı́n

doi:10.1002/bdrb.20182

Cited by 10 publications

(5 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We therefore challenged the second hypothesis by adding an NO donating drug (DETA/NO, 10 µM), however, cloned embryos did not benefit (DETA/NO, 28/80 blastocysts; control, 33/81; Fisher's exact test, p = 0.517). We conclude that the beneficial effect of arginine to cloned embryo pre-implantation development is probably not due to its conversion to NO but to other products such as polyamines [55], [58] or due to altered signaling pathways, for example, mTOR [59], [60].…”

Section: Resultsmentioning

confidence: 85%

Nuclear Reprogramming: Kinetics of Cell Cycle and Metabolic Progression as Determinants of Success

et al. 2012

View full text Add to dashboard Cite

Establishment of totipotency after somatic cell nuclear transfer (NT) requires not only reprogramming of gene expression, but also conversion of the cell cycle from quiescence to the precisely timed sequence of embryonic cleavage. Inadequate adaptation of the somatic nucleus to the embryonic cell cycle regime may lay the foundation for NT embryo failure and their reported lower cell counts. We combined bright field and fluorescence imaging of histone H2b-GFP expressing mouse embryos, to record cell divisions up to the blastocyst stage. This allowed us to quantitatively analyze cleavage kinetics of cloned embryos and revealed an extended and inconstant duration of the second and third cell cycles compared to fertilized controls generated by intracytoplasmic sperm injection (ICSI). Compared to fertilized embryos, slow and fast cleaving NT embryos presented similar rates of errors in M phase, but were considerably less tolerant to mitotic errors and underwent cleavage arrest. Although NT embryos vary substantially in their speed of cell cycle progression, transcriptome analysis did not detect systematic differences between fast and slow NT embryos. Profiling of amino acid turnover during pre-implantation development revealed that NT embryos consume lower amounts of amino acids, in particular arginine, than fertilized embryos until morula stage. An increased arginine supplementation enhanced development to blastocyst and increased embryo cell numbers. We conclude that a cell cycle delay, which is independent of pluripotency marker reactivation, and metabolic restraints reduce cell counts of NT embryos and impede their development.

show abstract

Section: Resultsmentioning

confidence: 85%

Nuclear Reprogramming: Kinetics of Cell Cycle and Metabolic Progression as Determinants of Success

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Serum putrescine level is significantly correlated with www.nature.com/scientificreports www.nature.com/scientificreports/ the level of glycosylated hemoglobin 28 . Putrescine partially prevents the dysmorphogenic effects of high glucose in rat embryos 29 . Guanidinoacetate was observed to be significantly decreased in the serum, urinary tract, and renal cortex of diabetic rats 30 .…”

Section: Discussionmentioning

confidence: 94%

Integrated metabolome analysis reveals novel connections between maternal fecal metabolome and the neonatal blood metabolome in women with gestational diabetes mellitus

Zhao¹,

Ge²,

Li³

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Gestational Diabetes Mellitus (GDM), which is correlated with changes in the gut microbiota, is a risk factor for neonatal inborn errors of metabolism (ieMs). Maternal hyperglycemia exerts epigenetic effects on genes that encode IEM-associated enzymes, resulting in changes in the neonatal blood metabolome. However, the relationship between maternal gut microbiota and the neonatal blood metabolome remains poorly understood. this study aimed at understanding the connections between maternal gut microbiota and the neonatal blood metabolome in GDM. 1H-NMR-based untargeted metabolomics was performed on maternal fecal samples and targeted metabolomics on the matched neonatal dry blood spots from a cohort of 40 pregnant women, including 22 with GDM and 18 controls. Multi-omic association methods (including Co-Inertia Analysis and Procrustes Analysis) were applied to investigate the relationship between maternal fecal metabolome and the neonatal blood metabolome. Both maternal fecal metabolome and the matched neonatal blood metabolome could be separated along the vector of maternal hyperglycemia. A close relationship between the maternal and neonatal metabolomes was observed by multi-omic association approaches. Twelve out of thirty-two maternal fecal metabolites with altered abundances from 872 1H-NMR features (Bonferroni-adjusted P < 0.05) in women with GDM and the controls were identified, among which 8 metabolites contribute (P < 0.05 in a 999-step permutation test) to the close connection between maternal and the neonatal metabolomes in GDM. Four of these eight maternal fecal metabolites, including lysine, putrescine, guanidinoacetate, and hexadecanedioate, were negatively associated (Spearman rank correlation, coefficient value < −0.6, P < 0.05) with maternal hyperglycemia. Biotin metabolism was enriched (Bonferroni-adjusted P < 0.05 in the hypergeometric test) with the four-hyperglycemia associated fecal metabolites. the results of this study suggested that maternal fecal metabolites contribute to the connections between maternal fecal metabolome and the neonatal blood metabolome and may further affect the risk of IEMs. Gestational diabetes mellitus (GDM) has attracted worldwide public health concern due to its adverse maternal, fetal and neonatal outcomes. GDM is a serious pregnancy complication with various risk factors 1 , including overweight, obesity, a family history of diabetes, advanced maternal age, etc. GDM has been linked with an increased risk of inborn errors of metabolism (IEMs) in offspring 2,3. IEMs are caused by inherited genetic defects and can be influenced by environmental stimuli 4. Accumulating evidence suggests that maternal hyperglycemia is associated

show abstract

“…Also, it has been shown in studies using pregnant rats with experimentally induced DM1 and in in vitro systems with high glucose, that molecules with antioxidant activity can help to reduce or prevent the occurrence of embryo malformations. Thus, it has been found that vitamin C (Cederberg et al, 2001; Zaken, Kohen, & Ornoy, 2001), vitamin E (Gäreskog, Eriksson, & Wentzel, 2006; Wentzel & Eriksson, 2005; Zaken et al, 2001), N ‐acetylcysteine (Roest et al, 2007), resveratrol (Singh et al, 2011), α‐lipoic acid (Al‐Ghafli, Padmanabhan, Kataya, & Berg, 2004; Sugimura et al, 2009), folic acid (Gäreskog et al, 2006; Wentzel & Eriksson, 2005; Zabihi, Eriksson, & Wentzel, 2007), α‐linoleic acid (Chirino‐Galindo, Barrera‐Argüelles, Trejo‐González, Mejía‐Zepeda, & Palomar‐Morales, 2017), and the polyamines spermidine and spermine (Chirino‐Galindo, Baiza‐Gutman, Barrera‐Escorcia, & Palomar‐Morales, 2009; Chirino‐Galindo, Mejía‐Zepeda, & Palomar‐Morales, 2012; Méndez & Palomar‐Morales, 1999) could prevent or avoid embryo malformations.…”

Section: Introductionmentioning

confidence: 99%

Verbascoside‐enriched fraction from Buddleja cordata Kunth ameliorates the effects of diabetic embryopathy in an animal model

Chirino-Galindo

López-Quintero

Ramírez-Domínguez

et al. 2021

Birth Defects Research

View full text Add to dashboard Cite

Background The deleterious effects of diabetes mellitus (DM) over development are apparently due to an increase in oxidative stress. Some antioxidants could prevent developmental alterations produced by diabetic state. Extracts of plants of the genus Buddleja are used traditionally for Mexican indigens to ameliorate some diseases. The purpose of this work was to evaluate the effect of the extract of Buddleja cordata over diabetic embryopathy. Methods Two experimental approaches were used: an in vivo study and an in vitro model. In the first, rats were treated with streptozotocin, streptozotocin plus methanolic extract of B. cordata, or none. Females were sacrificed at gestational day (GD) 19, and biochemical clinical parameters were measured; also, the fetuses were obtained and morphologically analyzed. In the in vitro model, a verbascoside‐enriched fraction (VEF) of the extract was used in whole embryo culture in order to search for the mechanisms for embryoprotection effect over hyperglycemia‐induced malformations. Results In the in vivo experiments, B. cordata extract reduces the frequency and severity of fetal malformations produced by chemically induced diabetes, and additionally partially ameliorates the diabetic condition; in the in vitro model, both severity and frequency of embryo dysmorphogenesis were reduced by the VEF; also, this fraction reduces lipoperoxidation without affecting the activity of the antioxidant enzymes. Conclusion The results suggest that verbascoside of methanolic extract and enriched fraction can directly affect the redox state, and thus, prevents the embryotoxicity mediated by oxidative stress, in embryos of diabetic pregnancy.

show abstract

Polyamines protect rat embryo in vitro from high glucose‐induced developmental delay and dysmorphogenesis

Abstract: Polyamines directly protect the embryo from the toxic effect of high glucose concentration on growth and development, although the mechanism remains to be elucidated.

Cited by 10 publications

References 41 publications

Nuclear Reprogramming: Kinetics of Cell Cycle and Metabolic Progression as Determinants of Success

Nuclear Reprogramming: Kinetics of Cell Cycle and Metabolic Progression as Determinants of Success

Integrated metabolome analysis reveals novel connections between maternal fecal metabolome and the neonatal blood metabolome in women with gestational diabetes mellitus

Verbascoside‐enriched fraction from Buddleja cordata Kunth ameliorates the effects of diabetic embryopathy in an animal model

Contact Info

Product

Resources

About