Urinary prostasin excretion is associated with adiposity in nonhypertensive African-American adolescents

De Huang Guo, Samip J. Parikh, Julie Chao, Norman K. Pollock, Xiaoling Wang, Harold Snieder, Gerjan Navis, James G. Wilson, Jigar Bhagatwala, Haidong Zhu, Yanbin Dong

Research output: Contribution to journalArticle

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Abstract

Background: Metabolic abnormalities in obesity can overstimulate the renal epithelial sodium channel (ENaC) and subsequently lead to blood pressure (BP) elevation. Prostasin, a membrane-bound/secretive serine protease, is thought to activate ENaC via the proteolytic cleavage of the channel. Our specific aim was to explore whether there is a relationship between adiposity and urinary prostasin excretion at the population level.Methods: In 271 African-American adolescents, urinary prostasin concentrations were determined by enzyme-linked immunosorbent assay and normalized by urinary creatinine.Results: Urinary prostasin excretion increased in the overweight/obese group (n = 110, 38.2 ± 4.0 ng/mg) vs. the normal-weight group (n = 161, 20.7 ± 1.2 ng/mg, P = 0.03). Urinary prostasin excretion was significantly correlated with BMI percentiles (r = 0.14, P = 0.02), waist circumference (r = 0.13, P = 0.05), total body fat mass (r = 0.20, P < 0.01), and percentage body fat (r = 0.23, P < 0.01). Urinary prostasin excretion was also correlated with plasma aldosterone (r = 0.11, P = 0.05) and systolic BP (SBP; r = 0.15, P = 0.02), but the significances disappeared after adjustment of any of the adiposity variables.Conclusion: Our data for the first time suggest that adiposity plays a role in urinary prostasin excretion, and its associations with aldosterone and BP appear to be modulated by adiposity. Whether urinary prostasin excretion is a biomarker/mechanism underlying obesity-related hypertension deserves further investigations.

Original languageEnglish (US)
Pages (from-to)206-210
Number of pages5
JournalPediatric research
Volume74
Issue number2
DOIs
StatePublished - Aug 1 2013

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Adiposity
African Americans
Blood Pressure
Aldosterone
Adipose Tissue
Obesity
Epithelial Sodium Channels
prostasin
Waist Circumference
Serine Proteases
Creatinine
Biomarkers
Enzyme-Linked Immunosorbent Assay
Hypertension
Kidney
Weights and Measures
Membranes
Population

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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Urinary prostasin excretion is associated with adiposity in nonhypertensive African-American adolescents. / Guo, De Huang; Parikh, Samip J.; Chao, Julie; Pollock, Norman K.; Wang, Xiaoling; Snieder, Harold; Navis, Gerjan; Wilson, James G.; Bhagatwala, Jigar; Zhu, Haidong; Dong, Yanbin.

In: Pediatric research, Vol. 74, No. 2, 01.08.2013, p. 206-210.

Research output: Contribution to journalArticle

Guo, De Huang ; Parikh, Samip J. ; Chao, Julie ; Pollock, Norman K. ; Wang, Xiaoling ; Snieder, Harold ; Navis, Gerjan ; Wilson, James G. ; Bhagatwala, Jigar ; Zhu, Haidong ; Dong, Yanbin. / Urinary prostasin excretion is associated with adiposity in nonhypertensive African-American adolescents. In: Pediatric research. 2013 ; Vol. 74, No. 2. pp. 206-210.
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T1 - Urinary prostasin excretion is associated with adiposity in nonhypertensive African-American adolescents

AU - Guo, De Huang

AU - Parikh, Samip J.

AU - Chao, Julie

AU - Pollock, Norman K.

AU - Wang, Xiaoling

AU - Snieder, Harold

AU - Navis, Gerjan

AU - Wilson, James G.

AU - Bhagatwala, Jigar

AU - Zhu, Haidong

AU - Dong, Yanbin

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N2 - Background: Metabolic abnormalities in obesity can overstimulate the renal epithelial sodium channel (ENaC) and subsequently lead to blood pressure (BP) elevation. Prostasin, a membrane-bound/secretive serine protease, is thought to activate ENaC via the proteolytic cleavage of the channel. Our specific aim was to explore whether there is a relationship between adiposity and urinary prostasin excretion at the population level.Methods: In 271 African-American adolescents, urinary prostasin concentrations were determined by enzyme-linked immunosorbent assay and normalized by urinary creatinine.Results: Urinary prostasin excretion increased in the overweight/obese group (n = 110, 38.2 ± 4.0 ng/mg) vs. the normal-weight group (n = 161, 20.7 ± 1.2 ng/mg, P = 0.03). Urinary prostasin excretion was significantly correlated with BMI percentiles (r = 0.14, P = 0.02), waist circumference (r = 0.13, P = 0.05), total body fat mass (r = 0.20, P < 0.01), and percentage body fat (r = 0.23, P < 0.01). Urinary prostasin excretion was also correlated with plasma aldosterone (r = 0.11, P = 0.05) and systolic BP (SBP; r = 0.15, P = 0.02), but the significances disappeared after adjustment of any of the adiposity variables.Conclusion: Our data for the first time suggest that adiposity plays a role in urinary prostasin excretion, and its associations with aldosterone and BP appear to be modulated by adiposity. Whether urinary prostasin excretion is a biomarker/mechanism underlying obesity-related hypertension deserves further investigations.

AB - Background: Metabolic abnormalities in obesity can overstimulate the renal epithelial sodium channel (ENaC) and subsequently lead to blood pressure (BP) elevation. Prostasin, a membrane-bound/secretive serine protease, is thought to activate ENaC via the proteolytic cleavage of the channel. Our specific aim was to explore whether there is a relationship between adiposity and urinary prostasin excretion at the population level.Methods: In 271 African-American adolescents, urinary prostasin concentrations were determined by enzyme-linked immunosorbent assay and normalized by urinary creatinine.Results: Urinary prostasin excretion increased in the overweight/obese group (n = 110, 38.2 ± 4.0 ng/mg) vs. the normal-weight group (n = 161, 20.7 ± 1.2 ng/mg, P = 0.03). Urinary prostasin excretion was significantly correlated with BMI percentiles (r = 0.14, P = 0.02), waist circumference (r = 0.13, P = 0.05), total body fat mass (r = 0.20, P < 0.01), and percentage body fat (r = 0.23, P < 0.01). Urinary prostasin excretion was also correlated with plasma aldosterone (r = 0.11, P = 0.05) and systolic BP (SBP; r = 0.15, P = 0.02), but the significances disappeared after adjustment of any of the adiposity variables.Conclusion: Our data for the first time suggest that adiposity plays a role in urinary prostasin excretion, and its associations with aldosterone and BP appear to be modulated by adiposity. Whether urinary prostasin excretion is a biomarker/mechanism underlying obesity-related hypertension deserves further investigations.

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