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A new crossover trial suggests that men with type 2 diabetes may have a broken communication line between their gut and kidneys when it comes to handling sodium. Healthy individuals excreted more sodium after swallowing a salt load than after receiving one intravenously — but men with T2D showed no such difference. Even a GLP-1 receptor agonist (exenatide) failed to restore this response.
Your gut and kidneys are supposed to talk to each other. When you eat a salty meal, the gut is thought to send a signal to the kidneys to ramp up sodium excretion — a process called gut-kidney feed-forward signalling. A new crossover trial published in Clinical Kidney Journal suggests that this communication may be broken in men with type 2 diabetes (T2D).
In the study, healthy individuals excreted significantly more sodium in the two hours after an oral salt load compared to an intravenous one — confirming the gut-kidney signalling pathway works as expected. But men with T2D showed no such difference, regardless of how the sodium was delivered. Researchers also tested whether exenatide, a GLP-1 receptor agonist, could jumpstart this signalling — it didn't.
By the Numbers:
Why it matters: Impaired gut-kidney signalling could help explain why people with T2D are more prone to salt-sensitive hypertension and kidney complications. Understanding — and potentially restoring — this pathway may open new doors for cardiorenal protection in diabetic patients.