Potassium supplementation blunts the effects of high salt intake on serum retinol‐binding protein 4 levels in healthy individuals

Aims/Introduction Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol‐binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte‐derived “signal” that plays the crucial role in salt‐related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. Materials and Methods A total of 42 participants (aged 25–50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low‐salt (7 days; 3 g/day NaCl) and high‐salt (7 days; 18 g/day) diets, and a high‐salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme‐linked immunosorbent assay. Results High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive ( r  = 0.528, P  < 0.01) and negative ( r  = −0.506, P  < 0.01) associations with 24‐h urinary sodium‐ and potassium excretion levels. Conclusions RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt‐induced insulin resistance or type 2 diabetes mellitus.