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University of Groningen Gestational diabetes mellitus and fetoplacental vasculature alterations Silva Lagos, Luis

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University of Groningen

Gestational diabetes mellitus and fetoplacental vasculature alterations Silva Lagos, Luis

DOI:

10.33612/diss.113056657

IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below.

Document Version

Publisher's PDF, also known as Version of record

Publication date: 2020

Link to publication in University of Groningen/UMCG research database

Citation for published version (APA):

Silva Lagos, L. (2020). Gestational diabetes mellitus and fetoplacental vasculature alterations: Exploring the role of adenosine kinase in endothelial (dys)function. University of Groningen.

https://doi.org/10.33612/diss.113056657

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Propositions

1. There is a strong link between the biological activities of adenosine and insulin. The complete understanding the link between the biological activities of adenosine and insulin seems promising and might result in new treatment strategies for diseases related to altered insulin signaling. (Chapter 3)

2. Insulin therapy as a treatment for GDM is not sufficient to prevent alterations in the fetoplacental vasculature. (Chapter 4)

3. It is difficult to study the natural history of GDM since GDM is usually (if not always) accompanied by other confounding factors (Chapter 4)

4. Adenosine signaling and adenosine as a regulator of methylation reactions are linked through adenosine kinase. (Chapter 5)

5. The nuclear isoform of adenosine kinase predominates in human umbilical vein endothelial cells (Chapter 6)

6. The expression of adenosine kinase (AK), human equilibrative nucleoside transporter 1 (hENT1) and S-adenosylhomocysteine hydrolase (SAHH) is sensitive to changes in glucose levels but seems to be independent of variations in adenosine levels. (Chapter 6)

7. High glucose (or hyperglycemia) is not sufficient to induce the endothelial dysfunction observed in the fetoplacental vasculature in GDM pregnancies. (Chapter 7)

8. The inhibition of adenosine kinase alleviates the endothelial inflammation induced by TNF-⍺. (Chapter 8)

9. High glucose induces a decreased oxygen consumption rate in human umbilical vein endothelial cells , indicating cellular senescence (Chapter 9)

10. Intrauterine exposure to detrimental factors conditions the offspring's health later in life. (In utero programming of chronic diseases. D. Barker. Clinical Science, 1998)

11. The road towards becoming a PhD is full of stones. Passion is what will keep you moving forward and will hold you up when you feel that you are about to fall.

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