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Serum Fibroblast Growth Factor 23 Levels are Associated with Vascular Smooth Muscle Dysfunction in Type 2 Diabetes
Yuka Natsuki1, Tomoaki Morioka1, Yoshinori Kakutani1
1Department of Metabolism, Endocrinology and Molecular Medicine, Osaka Metropolitan University Graduate School of Medicine.
High serum FGF23 levels are linked to impaired vascular smooth muscle function in type 2 diabetes patients, especially those with normal kidney function. This suggests FGF23 may indicate vascular dysfunction.
Area of Science:
- Endocrinology
- Nephrology
- Cardiovascular Medicine
Background:
- Elevated serum fibroblast growth factor 23 (FGF23) is linked to phosphate metabolism abnormalities in chronic kidney disease (CKD).
- FGF23 is also associated with cardiovascular disease risk, even in individuals without CKD.
- The relationship between FGF23 and vascular function in type 2 diabetes (T2D) requires further investigation.
Purpose of the Study:
- To investigate the association between serum FGF23 levels and vascular function in patients with T2D.
- To evaluate the impact of FGF23 on vascular endothelial and smooth muscle functions.
Main Methods:
- Cross-sectional study of 283 Japanese patients with T2D.
- Assessment of brachial artery flow-mediated dilatation (FMD) and nitroglycerin-mediated dilatation (NMD) using ultrasonography.
- Measurement of serum intact FGF23 levels via enzyme-linked immunosorbent assay.
Main Results:
- Serum FGF23 levels were inversely associated with NMD (vascular smooth muscle function), but not FMD (endothelial function).
- This association was independent of traditional atherosclerotic risk factors, estimated glomerular filtration rate (eGFR), and serum phosphate.
- The inverse relationship between FGF23 and NMD was more pronounced in patients with normal kidney function (eGFR ≥ 60 mL/min/1.73 m²).
Conclusions:
- Serum FGF23 levels are independently and inversely associated with vascular smooth muscle dysfunction in T2D patients.
- Increased FGF23 may serve as a novel biomarker for vascular smooth muscle dysfunction in T2D, particularly in those with preserved kidney function.
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