Abstract 2370: Brain Natriuretic Peptide Enhances Adiponectin Production in Adipocytes
Background. Adiponectin is a circulating adipose-derived cytokine that provides cardiovascular protection as well as anti-diabetic actions. Although adiponectin is down-regulated in patients with metabolic syndrome, the recent report shows that the pathophysiology of chronic heart failure (CHF) elevates the plasma adiponectin levels in patients with CHF, and that there is a tight linkage between the plasma adiponectin and BNP levels, culminating the idea that BNP regulates adiponectin production. We tested this hypothesis.
Methods and Results. In cultured 3T3-L1 adipocytes, BNP enhanced the mRNA expression in a dose- dependent manner (BNP concentrations; 0, 10-10, 10-9, and 10-8 mol/L: 1.00±0.04, 1.04±0.05, 1.16±0.06, and 1.40±0.03, respectively), which was prevented by the treatment with HS142–1 (1.05±0.02), a functional GC-A type receptor antagonist. Secretion of adiponectin into the media also was increased by the treatment with BNP. Furthermore, these effects were mediated through the cGMP-dependent manner. To confirm this effect of BNP in vivo, we administered rat BNP (0.2 μg/kg/min) to GC-A deficient (GC-A−/−) mice and their wild-type (GC-A+/+) littermates using osmotic pumps for 14 days. BNP significantly increased the plasma adiponectin concentrations in GC-A+/+ mice but not GC-A−/− mice (sham GC-A+/+, sham GC-A−/−, BNP GC-A+/+, and BNP GC-A−/−: 3.39±0.24, 4.11±0.15, 3.08±0.12, and 3.16±0.11 μg/mL, respectively), which was the case with mRNA levels in the adipose tissues of mice.
Conclusion. We conclude that BNP enhances adiponectin production in adipocytes, and BNP is a potential regulator of adiponectin production. This action may contribute to the elevated adiponectin concentration in patients with chronic heart failure.