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 Disclosure A. Asmar: None. P.K. Cramon: None. C.M. Sorensen: None. S. Madsbad: None. C. Moro: None. B. Hartmann: None. J.J. Holst: Advisory Panel; Self; Novo Nordisk A/S. B.L. Jensen: None. M. Asmar: None.