When you eat, your body sends extra blood to the gut to handle the incoming meal. New work puts a number on how much of that after-meal surge is driven by one specific gut hormone, and the number is not zero even in people whose diabetes was supposed to have blunted it.
In ten adults with type 2 diabetes, drinking a 75-gram glucose load raised blood flow through the superior mesenteric artery, the main vessel feeding the intestine, by 57 percent (95 percent confidence interval 26 to 88). When the same people got an intravenous infusion of a compound that blocks the receptor for glucose-dependent insulinotropic polypeptide, better known as GIP ↗, the surge came in about 15 percent lower (p=0.012). Block the hormone, and the meal-time blood rush to the gut partly deflates. The study appeared July 2 in Diabetologia ↗.
GIP is one of the two incretin hormones the gut releases after a meal. The other, GLP-1, is the one everyone has heard of by now. GIP matters here for a concrete commercial reason: tirzepatide ↗, sold as Mounjaro and Zepbound, hits the GIP receptor ↗ and the GLP-1 receptor at once, and it is the best-selling drug of its class. What GIP actually does in the body beyond nudging insulin has been genuinely unsettled. Companies have chased both GIP agonists and GIP blockers for weight loss and gotten weight loss from each, the kind of contradiction that means the hormone has jobs nobody has fully mapped.
Steering blood to the gut is one of those jobs. In healthy lean people, earlier work from the same Copenhagen group found endogenous GIP drives most of the after-meal rise in gut blood flow. In type 2 diabetes that vascular response to GIP is known to be impaired, sometimes gone entirely, which is what makes the new result worth reading: even in that impaired setting, blocking GIP still measurably cut the surge. The residual role survives the disease.
The mechanics. Researchers at Rigshospitalet in Copenhagen, led by Rasmus S. Rasmussen, ran a randomized, placebo-controlled crossover. The ten participants, adults aged 20 to 80 with an HbA1c between 48 and 75 millimoles per mole, came in four times and got oral glucose or plain water, each paired with either the GIP-receptor blocker GIP(3-30) or saline. Blood flow was tracked with phase-contrast MRI in three abdominal vessels: the superior mesenteric artery, the coeliac trunk, and the portal vein. Liver volume, liver oxygenation, and gallbladder volume were measured too. Alongside the smaller blood-flow surge, blocking GIP also lowered insulin and C-peptide, the standard readout of how hard the pancreas is working, while glucagon and blood glucose held steady. The trial was funded by the Novo Nordisk Foundation, whose namesake company sells the competing GLP-1 drug semaglutide.
The honest limits are small-study limits. Ten people is enough for a within-person physiology signal and too few for anything about outcomes. The single-blind design left the investigators aware of who got what. And the 15 percent figure is a real dent, not an abolition, so GIP is one contributor to the after-meal surge, not the whole of it. What the study adds is a concrete, MRI-measured vascular action for a hormone whose non-insulin jobs are still being argued over, in exactly the patients whose drugs now target its receptor.