1956-P: Increased Salt Intake Amplifies the Postprandial Glucagon-Like Peptide-1 Secretion

We have previously demonstrated that physiologically relevant changes in circulating glucagon-like peptide-1 (GLP-1) elicit a rapid increase in renal sodium excretion during intravenous sodium loading. The present study was designed to investigate the hypothesis that postprandial GLP-1 secretion is sensitive to dietary salt intake and is part of a feedforward natriuretic system. Under fixed sodium intake, 11 lean healthy males were examined twice in random order. Arterial blood samples were collected in 10-20 min intervals for 140 minutes after 75-g oral glucose load vs. 75-g oral glucose + 6-g oral salt load. Subjects remained supine during the experiments. Prior to each experiment, all subjects conducted a 4-day standardized diet with fixed salt intake and 24-h urine collections were completed successfully with urinary sodium excretions being similar between subjects (116±10 mmol). Arterial GLP-1 levels increased transiently in both studies and were higher around 80 min after the glucose+salt load compared to glucose alone (46 ± 4 pmol/L vs. 33 ± 3 pmol/L, p=0.011). The postprandial increase in arterial CCK levels was reduced by the glucose+salt load throughout the study (1.9 ± 0.1 pmol/L vs. 2.8 ± 0.2 pmol/L, p<0.001), whereas arterial GIP and gastrin levels increased transiently and similarly in both studies. The transient increase in arterial glucose, insulin and c-peptide levels were similar on both study days. Arterial renin and aldosterone levels did not change within subjects and between study days, whereas angiotensin II was significantly reduced around 80 min after the glucose+salt load (10.9 ± 1.5 pg/mL vs. 14.4 ± 1.5 pg/mL, p=0.004). Arterial proANP, ANP, and BNP levels remained unchanged on both days. This study demonstrates that an increased salt intake amplifies the postprandial GLP-1 secretion in healthy individuals, supporting a possible GLP-1-mediated feedforward natriuretic system, likely via a suppression of angiotensin II.