Key result
Elevated ET-1 is linked to lower adiponectin in obese children via direct synthesis inhibition.
Why the study?
The relationship between endothelial dysfunction and hypoadiponectinemia in pediatric obesity and the role of endothelin-1 in impairing adiponectin production remain unclear.
Does elevated ET-1 contribute to hypoadiponectinemia and impaired adiponectin-mediated vasodilation in pediatric obesity?
Comparison
Exposure of adipocytes to exogenous ET-1 or serum from overweight/obese children versus serum from lean children
Design
Cross-sectional study with in vitro adipocyte stimulation and ex vivo rat artery assays
Authors
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ET-1 may drive hypoadiponectinemia in obese children; leaves open whether blockade restores adiponectin-mediated vasodilation.
Cross-Sectional (n=60)
Does elevated ET-1 contribute to hypoadiponectinemia and impaired adiponectin-mediated vasodilation in pediatric obesity?
p-value: p=<0.001
Elevated ET-1 in childhood obesity directly inhibits adiponectin synthesis via MAPK signaling, providing a mechanistic link between pediatric obesity and cardiovascular complications.
Nacci et al. (2013) conducted a cross-sectional in Pediatric obesity (n=60). Elevated Endothelin-1 (ET-1) levels vs. Lean children was evaluated on Total and high-molecular-weight adiponectin and ET-1 levels (p=<0.001). Elevated ET-1 levels in overweight and obese children were significantly associated with decreased adiponectin levels (P<0.001), with ET-1 directly inhibiting adiponectin synthesis in vitro.
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