1378-P: Habitual High Sodium Intake Is Associated with Alterations in Glucose Homeostasis Including GLP-1 Secretion

Abstract

Objective: Although epidemiological studies robustly confirm the impact of a high sodium diet (HSD) in hypertension, the effect of HSD on glucose homeostasis and gut hormones has not been fully elucidated. We hypothesize that the metabolic effects of a HSD might be modulated by changes in the gut microbiome, as it was recently identified as a salt-sensitive compartment. Methods: A cross-sectional analysis was carried out in 120 adults with metabolic syndrome traits (60 ± 7 years, BMI 31.1 kg/m2, 42% male). Dietary habits were assessed using a Food Frequency Questionnaire. Participants were divided into two groups (normal sodium diet (NSD) vs. HSD) with a cut off value of < 2400 mg/d for NSD and ≥ 2400 mg/d for HSD, according to the recommended maximum intake for sodium by the German Nutrition Society. Fasting and postprandial blood samples were taken after performing an oral glucose tolerance test (OGTT) over 180 min for metabolic characterization, HOMA-IR was calculated. Gut microbiome composition was analyzed using 16S rRNA amplicon sequencing. Linear models were used to test for differences between HSD and NSD in metabolic parameters. Results: Participants of the HSD group had higher fasting GLP-1 levels (p < 0.05) in comparison to NSD, while the GLP-1 incremental area under the curve during OGTT was lower (p < 0.01). In females, HOMA-IR was higher in the HSD group compared to the NSD group. Bacterial α- and β-diversity did not differ between groups. However, several bacterial taxa correlated with metabolic parameters. In HSD, Streptococcaceae and Veillonellaceae were positively associated with HOMA-IR, and Parabacteroides were inversely correlated with fasting GLP-1. Conclusion: This analysis provides evidence that a HSD affects insulin resistance and GLP-1 secretion possibly modulated by specific bacterial taxa. Our results add on findings indicating an adverse impact of sodium intake on the development of diabetes, possibly with sex-specific differences. Disclosure A.Donkers: None. P.Stehle: None. M.Simon: None. H.Huber: None. A.Schieren: None. A.Mantri: None. W.Seel: None. B.Stoffel-wagner: None. M.Coenen: None. P.Krawitz: None. J.J.Holst: Advisory Panel; Novo Nordisk A/S, Eli Lilly and Company, Board Member; Bainan Biotech, Antag Therapeutics, Consultant; Alphasights, Eli Lilly and Company, ShouTi Pharma Inc., Zealand Pharma A/S, Other Relationship; Novo Nordisk, Novo Nordisk Pharma, Mayo Clinic, Boehringer-Ingelheim, Scohia Pharma Inc., Research Support; ARLA, European Union, Novo Nordisk Foundation.