Abstract
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.