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Obesity (Silver Spring). 2014 Jun;22(6):1470-6. doi: 10.1002/oby.20716. Epub 2014 Feb 19.

High-salt intake induced visceral adipose tissue hypoxia and its association with circulating monocyte subsets in humans.

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Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury Institute of Cardiovascular Disease and Heart Center Pingjin Hospital, Logistics University of the Chinese People's Armed Police Forces, Tianjin, China.



To investigate the feasibility of blood oxygen level dependent magnetic resonance imaging (BOLD-MRI) in evaluating human visceral adipose tissue (AT) oxygenation induced by salt loading/depletion and its association with changes in circulating monocyte subsets.


A dietary intervention study was performed in 23 healthy volunteers beginning with a 3-day usual diet followed by a 7-day high-salt diet (≥15 g NaCl/day) and a 7-day low-salt diet (≤5 g NaCl/day). BOLD-MRI was used to evaluate oxygenation in perirenal AT.


Salt loading led to a consistent AT hypoxia (increase in the R2* signal, 25.2 ± 0.90 s(-1) vs. baseline 21.5 ± 0.71 s(-1) , P < 0.001) and suppression of circulating renin-angiotensin-aldosterone system (RAAS), as well as an expansion of the CD14++CD16+ monocytes and monocyte pro-inflammatory activation. In salt depletion phase, the hypoxic state of AT and the expanded CD14++CD16+ monocyte pool were regressed to baseline levels, accompanied by a rebound activation of RAAS. Moreover, AT oxygenation level was positively correlated with the CD14++CD16+ monocytes (r = 0.419, P < 0.001).


This work provides proof-of-principle evidence supporting the feasibility of BOLD-MRI in monitoring visceral AT oxygenation in humans induced by dietary salt loading/depletion. In addition, the CD14++CD16+ monocytes may participate in the pathogenesis of high-salt intake induced AT hypoxia.

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