Why the study?
Do patients with GCK and HNF1A-MODY have increased intima-media thickness and endothelial dysfunction compared to nondiabetic controls?
Population
169 subjects, including 64 with GCK gene mutations, 52 with HNF1A gene mutations, and 53 nondiabetic…
Comparison
Presence of GCK or HNF1A gene mutations (MODY) vs Nondiabetic controls
Design
Cross-sectional
Key result
HNF1A-MODY and GCK-MODY patients had significantly lower flow-mediated dilatation than controls (9.9% and 11.1% vs 13.9%; P=0.0001), and HNF1A-MODY patients had higher intima-media thickness.
Authors
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Endothelial dysfunction in GCK- and HNF1A-MODY may signal early vascular risk; hypothesis-generating and leaves open need for longitudinal outcome studies.
Cross-Sectional (n=169)
Do patients with GCK and HNF1A-MODY have increased intima-media thickness and endothelial dysfunction compared to nondiabetic controls?
p-value: p=0.008
Patients with HNF1A-MODY exhibit early atherosclerotic phenotypes with increased IMT, and both GCK and HNF1A-MODY patients show evidence of endothelial dysfunction compared to healthy controls.
Szopa et al. (2014) conducted a cross-sectional in Maturity-onset diabetes of the young (MODY) (n=169). GCK and HNF1A gene mutations vs. Nondiabetic controls was evaluated on Carotid artery intima-media thickness (IMT) and endothelial function assessed by brachial artery flow-mediated dilatation (FMD) (p=0.008). HNF1A-MODY and GCK-MODY patients had significantly lower flow-mediated dilatation than controls (9.9% and 11.1% vs 13.9%; P=0.0001), and HNF1A-MODY patients had higher intima-media thickness.