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September 14, 2026Clinical Kidney JournalOpen Access

Oral sodium loading fails to increase 24-hour natriuresis vs intravenous loading in T2D despite exenatide.

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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

CMCharlotte M MosterdBWBritt Eveline WeverMBMichiel J B van Baar

Discussion

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Overview

GLP-1RA may restore impaired oral natriuresis in T2D men; leaves open clinical relevance and generalizability.

Key Points

  • To investigate whether gut-kidney feed-forward sodium regulation is impaired in individuals with type 2 diabetes and whether glucagon-like peptide-1 receptor agonism restores this response.
  • Mechanistic, randomized, double-blind, placebo-controlled crossover trial in 11 men with type 2 diabetes adhering to a standardized low-sodium diet (<90 mmol/day) for 7 days before visits.
  • Participants underwent three experimental conditions in random order with a 154 mmol sodium challenge: intravenous sodium loading (ISL), oral sodium loading with placebo (OSL-placebo), and oral sodium loading with exenatide infusion (OSL-exenatide).
  • The primary endpoint was cumulative 24-hour urinary sodium excretion, with secondary measures including fractional sodium excretion, glomerular filtration rate, and ambulatory blood pressure.
  • Median cumulative 24-hour sodium excretion did not differ significantly between ISL (105 mmol, IQR 55–156), OSL-placebo (101 mmol, IQR 71–134), and OSL-exenatide (100 mmol, IQR 63–123).
  • Early natriuretic responses, fractional sodium excretion, and both daytime and nighttime ambulatory blood pressures showed no differences across all three interventions.

Study Design

Type

RCT (n=11)

Blinding

double-blind

Randomization

randomized cross-over

Structured PICO

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?

P
Population
11 men with type 2 diabetes (mean age 60 years) who underwent three experimental sodium loading conditions in a cross-over design.
I
Intervention
Oral sodium loading (154 mmol) with concomitant exenatide infusion, or oral sodium loading (154 mmol) with placebo infusion.
C
Comparator
Intravenous sodium loading (154 mmol).
O
Outcome
Cumulative urinary sodium excretion over 24-hours.surrogate

Main Result

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.

Cite This Study

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.

synapsesocial.com/papers/6aa7afef79e9260bc85aace8https://doi.org/10.1093/ckj/sfag315
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