Leptin Is Associated with Serum Aldosterone in Overweight - Obese Children
Presentation Number: SUN 522
Date of Presentation: April 2nd, 2017
Carmen Campino*1, Rene Baudrand1, Andrea Vecchiola1, Cristian A Carvajal1, Carolina P Valdivia1, Cristobal A Fuentes1, Alejandra Tapia-Castillo1, Hernan Garcia1, Marlene Aglony2, Carolina Mendoza2, Carolina A Loureiro1, Francisca Grob1, Sandra Solari1, Fidel Allende1, Rodrigo Bancalari1, Carlos F Lagos1, Carlos E Fardella1 and Alejandro Martinez3
1Pontificia Universidad Catolica de Chile, Santiago, Chile, 2Pontificia Universidad Católica de Chile, Santiago, Chile, 3Pontificia Universidad Catolica de Chile, Santiago
Background: The excessive synthesis of aldosterone contributes to the development and progression of hypertension and metabolic and cardiovascular dysfunction. In obese, hyperleptinemia is associated with the development of hypertension. Leptin is a newly described regulator of aldosterone synthesis that acts directly on adrenal glomerulose cells to increse CYP11B2 expression and enhance aldosterone production in human adrenal cells lines and in animal models. Objetive: To analyse if there is association between leptin with serum aldosterone (SA), as well as with blood pressure (BP), plasma renin activity (PRA) and 24h-Na+/K+ urine ratio. Design: Cross sectional study. Subjects and Methods: We studied 77 subjects between 6.1 and 18 years old (mean, 13.2 years, 42 females). They were categorized in eutrophic (BMI p<85) and overweight-obese (BMI p≥85). After overnight fasting: antropometric parameters and blood pressure were measured, after at least 15 min of rest. Systolic (SBPi) and diastolic blood pressure index (DBPi) were calculated using the observed BP/50th percentile BP value for gender, age and stature. We also measured: SA, PRA, plasma and urinary (24h) Na+ and K+. The data corresponded to mean ± SD. They were analized by t test, Pearson correlation and multiple regression analysis. Results: The comparison between eutrophic (n=37, BMI-z= 0.37±0.49) and overweight-obese subjects (n=40, BMI-z=1.66 ± 0.39; p<0.001) showed SBPi=1.06 ± 0.11 vs 1.12 ± 0.12; p=0.012. DBPi=1.10 ± 0.15 vs 1.15 ± 0.16; p=0.185. Leptin (ng/ml): 6.7 ± 6.1 vs 15.5 ± 10.2; p<0.001. Aldosterone (ng/dl): 12.2 ± 8.9 vs 11.5 ± 6.4; p=0.711. PRA (ng/ml*h)=2.63 ± 2.36 vs 2.84 ± 1.67; p= 0.645. Urinary Na+ (mEq/g creatinine): 133 ± 59 vs 159 ± 86; p= 0.130. Urinary Na+/K+ ratio: 3.2 ± 2.0 vs 3.1± 1.5 p=0.638.In the group of overweight-obese subjects, leptine showed an possitive association with SA (r=0.415; p<0.001). After controlling by blood pressure, gender, age and Na+/K+ ratio, this association persisted (r=0.441, p= 0.012). No association was found between leptin with SBPi, DBPi, PRA and urinary Na+/K+ ratio. In eutrophic children no association was found between leptin and none of the variables studied. Conclusions: In overweight-obese children, the leptin concentration was positively associated with serum aldosterone. This association is independent of age, gender, blood pressure and urinary excretion of the Na+/K+ ratio. Our clinical results support the recently described effect of leptin on aldosterone secretion in human adrenal cell lines and in animal models.
Nothing to Disclose: CC, RB, AV, CAC, CPV, CAF, AT, HG, MA, CM, CAL, FG, SS, FA, RB, CFL, CEF, AM