ArticleClinical kidney journal2026
Gut-kidney signaling is impaired in individuals with type 2 diabetes.
Article in Clinical kidney journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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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/m 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.
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