Abstract
This thesis investigates the interaction between phosphate and glucose regulation and the impact of this interaction on the risk of cardiovascular diseases in people with diabetes. Phosphate appears to play a significant role in the development of cardiovascular diseases.
From the initial chapters of this thesis, it is clear that there is a strong interplay between phosphate and glucose regulation. During diabetic ketoacidosis (DKA), a severe manifestation of diabetes characterized by excessively high blood sugar levels, substantial fluctuations in phosphate levels occur. In healthy individuals too, after glucose intake, there are changes in phosphate levels and the primary phosphate-regulating hormone FGF23. Conversely, elevated levels of FGF23 are also linked to the risk of developing type 2 diabetes (T2D).
Subsequent studies explored the role of phosphate in the risk of cardiovascular diseases in T2D. In individuals with T2D, elevated phosphate levels are more strongly associated with an increased mortality risk compared to those without diabetes. Phosphate is a strong predictor in the onset of vascular calcification, and glucose may further intensify this effect. A faster "T50-time," indicative of developing vascular calcification in the future, is linked to the degree of glucose regulation in T2D (measured as HbA1c). This T50-time predicts mortality from cardiovascular diseases in these patients. The question is how to reduce phosphate levels. The final chapter indicates that a high dairy intake, rich in phosphate, does not result in higher phosphate levels.
From the initial chapters of this thesis, it is clear that there is a strong interplay between phosphate and glucose regulation. During diabetic ketoacidosis (DKA), a severe manifestation of diabetes characterized by excessively high blood sugar levels, substantial fluctuations in phosphate levels occur. In healthy individuals too, after glucose intake, there are changes in phosphate levels and the primary phosphate-regulating hormone FGF23. Conversely, elevated levels of FGF23 are also linked to the risk of developing type 2 diabetes (T2D).
Subsequent studies explored the role of phosphate in the risk of cardiovascular diseases in T2D. In individuals with T2D, elevated phosphate levels are more strongly associated with an increased mortality risk compared to those without diabetes. Phosphate is a strong predictor in the onset of vascular calcification, and glucose may further intensify this effect. A faster "T50-time," indicative of developing vascular calcification in the future, is linked to the degree of glucose regulation in T2D (measured as HbA1c). This T50-time predicts mortality from cardiovascular diseases in these patients. The question is how to reduce phosphate levels. The final chapter indicates that a high dairy intake, rich in phosphate, does not result in higher phosphate levels.
| Original language | English |
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| Qualification | Doctor of Philosophy |
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| Supervisors/Advisors |
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| Award date | 13-Dec-2023 |
| Place of Publication | [Groningen] |
| Publisher | |
| Print ISBNs | 978-94-6469-627-1 |
| DOIs | |
| Publication status | Published - 2023 |