High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome
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2014Metadata
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Baudrand, R.
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High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome
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Abstract
Objective High sodium (HS) diet is associated with hypertension
(HT) and insulin resistance (IR). We evaluated whether HS
diet was associated with a dysregulation of cortisol production
and metabolic syndrome (MetS).
Patients and measurements We recruited 370 adults
(18–85 years, BMI 29 3 4 4 kg/m2, 70% women, 72% HT,
61% MetS). HS diet (urinary sodium >150 mEq/day) was
observed in 70% of subjects. We measured plasma hormones,
lipid profile, urinary free cortisol (UFC) and cortisol tetrahydrometabolites
(THM).
Results Urinary sodium was correlated with UFC (r = +0 45,
P < 0 001), cortisol THM (r = +0 41, P < 0 001) and inversely
with adiponectin, HDL and aldosterone, after adjusting by age,
gender and BMI. Subjects with high, compared with adequate
sodium intake (50–149 mEq/day) had higher UFC (P < 0 001),
THM (P < 0 001), HOMA-IR (P = 0 04), HT (81% vs 50%,
P < 0 001), MetS (69% vs 41%, P < 0 001) and lower adiponectin
(P = 0 003). A multivariate predictive model adjusted by confounders
showed a high discriminative capacity for MetS (ROC
curve 0 878) using four clinical variables: HS intake [OR = 5 6
(CI 2 3–15 3)], HOMA-IR [OR 1 7 (1 3–2 2)] cortisol THM [OR
1 2 (1 1–1 4)] and adiponectin [OR = 0 9 (0 8–0 9)], the latter
had a protective effect.
Conclusions High sodium diet was associated with increased
urinary cortisol and its metabolites. Also, HS diet was associated
with HT, insulin resistance, dyslipidaemia and hypoadiponectinaemia,
even when adjusting by confounding variables. Further,
we observed that high salt intake, IR and higher cortisol metabolites,
alone or combined in a clinical simple model, accurately
predicted MetS status, suggesting an additive mechanism in
obesity-related metabolic disorders.
General note
Artículo de publicación ISI
Patrocinador
FONDEF D08I1087, Fondecyt 1100356, Fondecyt 1130427 and
Millennium Institute in Immunology and Immunotherapy
P09/016-F. CAC is a PhD fellow of CONICYT.
Quote Item
Clinical Endocrinology (2014) 80, 677–684
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