Why the study?
Whether the gut-kidney feed-forward mechanism that enhances natriuresis after oral sodium loading is impaired in type 2 diabetes and if GLP-1 receptor agonism can restore it remains unknown.
Does oral sodium loading or acute GLP-1 receptor agonism with exenatide improve natriuresis compared to intravenous sodium loading in men with type 2 diabetes?
Comparison
Oral sodium loading with exenatide infusion vs oral sodium loading with placebo vs intravenous sodium loading
Design
Randomized, double-blind, placebo-controlled cross-over trial
Follow-up
24 hours
Key result
Oral sodium loading did not increase 24-hour natriuresis compared to intravenous loading in men with type 2 diabetes (101 vs 105 mmol), and exenatide did not restore this gut-kidney response.
Authors
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GLP-1RA may restore impaired oral natriuresis in T2D men; leaves open clinical relevance and generalizability.
RCT (n=11)
double-blind
randomized cross-over
Does oral sodium loading or acute GLP-1 receptor agonism with exenatide improve natriuresis compared to intravenous sodium loading in men with type 2 diabetes?
Absolute Event Rate: 101% vs 105%
In men with type 2 diabetes, oral sodium loading does not induce greater natriuresis than intravenous loading, and acute GLP-1 receptor agonism with exenatide does not restore this impaired gut-kidney feed-forward mechanism.
Mosterd et al. (2026) conducted an RCT in type 2 diabetes (n=11). Oral sodium loading with placebo or exenatide vs. Intravenous sodium loading was evaluated on cumulative urinary sodium excretion over 24-hours. Oral sodium loading did not increase 24-hour natriuresis compared to intravenous loading in men with type 2 diabetes (101 vs 105 mmol), and exenatide did not restore this gut-kidney response.