SAT-388 The Influence of Dietary Sodium Intake on Cortisol and Glucose Homeostasis

Background: Glucose homeostasis is regulated by a range of physiological processes, including cortisol. Hypercortisolism and dietary sodium intake can influence glycemia and cardiovascular risk. Herein, we investigated the influence of dietary sodium intake on cortisol and glucose homeostasis. Methods: 630 participants free of cardiovascular disease were evaluated following one week of liberal dietary sodium intake (200 mmol/day) and again after one week of restricted dietary sodium intake (10 mmol/day). Following each diet, laboratory investigations included 24-hour urinary free cortisol (24hUFC), fasting morning serum cortisol, plasma glucose and insulin concentration. The effects of sodium intake on cortisol and glucose parameters were evaluated using paired t-tests. The association between cortisol and fasting plasma glucose was evaluated using linear regression with adjustment for sex, race, body mass index, blood pressure, diabetes status, urinary sodium excretion, serum aldosterone and plasma renin activity. Results: Participants ranged from 18 to 66 years old (mean 46.1 ± 10.6 years). Mean 24h urinary sodium excretion was 243.9 ± 68.1 mmol/day on the liberal sodium diet and 13.9 ± 9.8 mmol/day on the restricted sodium diet. When compared to restricted sodium intake, the liberal sodium intake decreased fasting plasma glucose (91.3 ± 15.4 vs. 95.0 ± 17.8 mg/dl, p <0.001) and insulin (10.4 ± 8.4 vs. 11.8 ± 8.3 μU/ml, p<0.001), but increased 24hUFC (64.5 ± 32.5 vs. 44.0 ± 23.8 μg/day, p<0.001). When participants consumed a liberal sodium diet, 24hUFC was positively associated with fasting plasma glucose (adjusted β = 0.05852 mcg per mg/dL, 95% CI: 0.02472 - 0.09233, p<0.001). In contrast, when participants consumed a restricted sodium diet, there was no association between 24hUFC and fasting plasma glucose. There was no association between serum cortisol and fasting plasma glucose on either dietary condition. Conclusions: Liberal dietary sodium intake increased 24hUFC and decreased fasting plasma glucose, when compared to restricted dietary sodium intake. Further, higher 24hUFC levels were associated with higher fasting plasma glucose values when participants consumed a liberal sodium, but not restricted sodium diet. Dietary sodium intake appears to modulate levels of 24hUFC, fasting glucose, and the relationship between cortisol and glucose in a manner that may have clinical and prognostic implications for the evaluation of glycemia and cardiovascular risk in the general population.