Gut-kidney signaling is impaired in individuals with type 2 diabetes
- Design
- Crossover trial
- Drugs
- Exenatide
- Assessment
- Not yet reviewed by a person · added Oct 18, 2026
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The source, as retrieved
Abstract
[BACKGROUND AND AIMS] In healthy individuals, oral sodium loading induces more rapid natriuresis than intravenous administration, suggesting a gut-kidney feed-forward mechanism. Whether this physiological response is impaired in type 2 diabetes (T2D), and whether pharmacological glucagon-like peptide-1 receptor agonism can restore it, remains unknown. [MATERIALS AND METHODS] We conducted a mechanistic, randomized, double-blind, placebo-controlled cross-over trial, in men with T2D. Participants adhered to a standardized sodium intake (<90 mmol/day) for 7 days before each study visit. Each participant underwent three experimental conditions in random order: (1) intravenous sodium loading (ISL), (2) oral sodium loading with placebo (OSL-placebo) infusion, and (3) OSL with concomitant exenatide infusion (OSL-exenatide). Each sodium load contained 154 mmol sodium. The primary endpoint was cumulative urinary sodium excretion over 24-h. Secondary endpoints included early natriuresis, fractional sodium excretion, ambulatory blood pressure, extracellular volume, and measured glomerular filtration rate. [RESULTS] Eleven men with T2D (mean age 60 ± 4.7 years, BMI 31.9 ± 3.9 kg/m2, HbA1c 7.5 ± 0.9%, systolic blood pressure 127 ± 22 mmHg) completed the study. Median cumulative 24 h sodium excretion did not differ significantly between ISL (105; IQR 55-156 mmol), OSL-placebo (101; 71-134 mmol), or OSL-exenatide (100; 63-123 mmol). Early natriuretic responses and fractional sodium excretion were similar across interventions. Daytime and nighttime blood pressure did not differ between interventions. [CONCLUSION] In contrast to observations in healthy individuals, OSL did not result in elevated natriuresis compared with ISL in T2D, consistent with impaired gut-kidney feed-forward regulation. Acute GLP-1R-activation with exenatide did not restore this response, suggesting additional entero-renal pathways mediate postprandial natriuretic regulation.