Long-term dietary sodium restriction increases adiponectin expression and ameliorates the proinflammatory adipokine profile in obesity

Abstract Background/aim Obesity is associated with changes in adiponectin and pro-inflammatory adipokines. Sodium intake can affect adipokine secretion suggesting a role in cardiovascular dysfunction. We tested if long-term dietary sodium restriction modifies the expression of adiponectin and ameliorates the pro-inflammatory profile of obese, diabetic mice. Methods/results Db/db mice were randomized to high sodium (HS 1.6% Na+, n  = 6) or low sodium (LS 0.03% Na+, n  = 8) diet for 16 weeks and compared with lean, db/+ mice on HS diet ( n  = 8). Insulin levels were 50% lower in the db/db mice on LS diet when compared with HS db/db ( p db/db mice by 5-fold when compared with db/db mice on HS diet and by 2-fold when compared with HS lean mice (both p db/db mice on HS diet, achieving levels similar to those of lean mice. MCP-1, IL-6 and TNF-α expression were reduced more than 50% in adipose tissue of db/db mice on LS diet when compared with HS db/db mice (all p db/db mice had significantly reduced circulating MCP-1 and IL-6 levels when compared with HS db/db mice (both p Conclusion In obese-diabetic mice, long-term LS diet increases adiponectin in heart and adipose tissue and reduces pro-inflammatory factors in adipose tissue and plasma. These additive mechanisms may contribute to the potential cardioprotective benefits of LS diet in obesity-related metabolic disorders.