Abstract
Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous
systems, both of which can increase insulin resistance (IR). We investigated the hypothesis
that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals
were studied after 7 days of LS diet (urine sodium <20 mmol/d) and 7 days of high-salt
(HS) diet (urine sodium >150 mmol/d) in a random order. Insulin resistance was measured
after each diet and compared statistically, unadjusted and adjusted for important
covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range,
18-65) and with body mass index of 25.3 ± 4.0 kg/m2, were included in this study. Mean (SD) homeostasis model assessment index was significantly
higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P < .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly
associated with higher homeostasis model assessment index independent of age, sex,
blood pressure, body mass index, serum sodium and potassium, serum angiotensin II,
plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine.
Low-salt diet is associated with an increase in IR. The impact of our findings on
the pathogenesis of diabetes and cardiovascular disease needs further investigation.
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Article Info
Publication History
Published online: November 01, 2010
Accepted:
September 11,
2010
Received:
July 23,
2010
Footnotes
Author contributions: RG conceived the idea, analyzed and interpreted the data, and wrote the manuscript; GHW helped in interpretation of data and reviewed the manuscript; SH helped with statistical analysis; NB recruited patients and reviewed the manuscript; PNH recruited patients and reviewed the manuscript; and GKA helped in interpretation of data and revised the manuscript.
Identification
Copyright
© 2011 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
