Your Gut Makes Its Own GLP-1. A 10-Person Tube Study Found a Chickpea’s Structure Changed When the Gut Hormones Arrived

A paper published in Nature Communications on September 15 describes one of the more demanding nutrition experiments of the year, and on September 23 it reached Yahoo Health. Ten healthy adults in London agreed to have thin tubes passed through the nose into the stomach, the duodenum and, on later visits, the far end of the small intestine. Then they ate the same chickpeas, prepared three ways, while researchers from Imperial College London and the Quadram Institute sampled each stretch of gut, hour by hour.

The short answer: the chickpeas’ physical structure changed where their starch was digested, and the gut’s hormone signals followed. When the plant cells had been broken open, sugars from starch appeared early and high in the gut and a hormone called GIP spiked fast. When the cells stayed intact, more starch and protein reached the ileum, the last stretch of the small intestine, and the hormones made there, GLP-1 and PYY, ran later and longer. Your gut makes its own GLP-1. This study shows a food’s form can shift when its signals arrive. It does not show food acting like a GLP-1 drug.

The studySame chickpeas, three structures

Every bowl started as 75 grams of dry chickpeas, according to the paper’s supplementary methods. For the broken-cell meal, soaked chickpeas were blended before cooking, which ruptures the cells. For the single-cell meal, they were cooked for 80 minutes until the cells came apart whole. For the cell-cluster meal, they were coarsely milled into semolina-sized pieces, then cooked. All three were served warm as a porridge with sugar-free jelly and jam, and each carried the same 30 grams of starch. None of it was hummus.

The trial ran in phases between 2020 and 2022. All ten volunteers first spent four days in hospital with tubes in the stomach and duodenum, eating one meal each morning in random order while blood and gut fluid were sampled for three hours; those results appeared in Nature Metabolism in June 2025. Eight returned for three more stays with a tube in the ileum, sampled hourly for eight hours, and a short visit collected chewed samples from the mouth. Funding was public, mainly from the UK’s Biotechnology and Biological Sciences Research Council, with no food-industry money listed. Three authors hold shares in Melico Sciences, which the paper says was not involved, and co-senior author Cathrina Edwards of the Quadram Institute declared in the 2025 paper that she is an inventor, executive director and shareholder of PulseON Food Ingredients; PulseON is the patented intact-cell chickpea flour developed at the Quadram Institute.

The hormonesWhy the address matters

The gut’s hormone-making cells are not spread evenly. A 2019 review by 25 GLP-1 researchers led by Timo Müller, some of them at Novo Nordisk and Janssen, describes GIP-making K-cells as most abundant high in the small intestine, and GLP-1-making L-cells as sparse there and densest in the ileum and colon; PYY comes from the same L-cells, the chickpea paper notes. The review cites a telling experiment: glucose dripped into the duodenum slowly enough to be absorbed on the spot released GIP but not GLP-1, while glucose delivered to the ileum released both.

That is what the chickpeas did. In the first phase, the broken-cell porridge sent blood sugar higher, with a peak rise 190% above the cell-cluster meal’s and 92% above the single-cell meal’s. GIP shot up within about 30 minutes of the broken meal but climbed slowly after the intact ones. GLP-1 peaked early after the broken meal and reached a similar height 84 minutes later after the single-cell meal. That meal left people feeling fullest, though they did not eat significantly less at an unlimited pasta meal four hours later. The authors say the one GLP-1 difference in total response should be interpreted “with caution.”

The new paper follows the meal further. In samples from the ileum, the intact meals still had starch and protein locked inside cells, while the broken-cell meal arrived as mostly empty cell walls. The intact meals delivered more glucose, maltose and amino acids to the ileum, and GLP-1 and PYY stayed up longer over the eight hours. The statistics are clearest for PYY, with an overall meal effect, although the individual time points that reached significance compared the two intact meals. For GLP-1 over those eight hours, the paper reports correlations with nutrients in the ileum but does not report a significant difference between meals.

The bacteriaMouth microbes along for the ride

The paper’s most unexpected finding has little to do with chickpea structure. While fasting, the ileum’s bacteria were dominated by Haemophilus and Streptococcus. After eating, mouth species such as Rothia and Gemella sanguinis rose. Comparing strain-level DNA from the saliva and ileum of five participants, the team found 106 strains in both. Strains shared with the mouth made up around 10% of ileal bacteria before eating, then peaked when the chickpea meal arrived and again after a standard pasta lunch, at as much as about half. That happened after all three meals. The authors propose that mouth bacteria ride down inside swallowed food, and some of these strains tracked with PYY.

Hold this one loosely. It rests on five people, saliva and ileum were sampled on different visits, and the tube passes through the nose and throat. The authors argue contamination is unlikely because the mouth strains rose with meals rather than steadily, but write that low-level contamination “cannot be fully excluded.” These were healthy volunteers, and nothing marks the pattern as a problem; it suggests the small intestine’s microbes shift more after a meal than fasting samples show.

What it meansNot a drug, and not a diet plan yet

Because GLP-1 is now a household word, precision helps. The GLP-1 your L-cells make is broken down fast: the Müller review puts its half-life at around one to two minutes, with only about 10 to 15% of the active hormone reaching general circulation. The medications are modified to resist that breakdown; the review lists one once-weekly drug’s half-life at 160 hours. Mingzhu Cai, first author of the 2025 paper and co-first author of the new one, said in Imperial’s 2025 release that “natural levels of GLP-1 will never reach that level of pharmaceutical dose.” Shifting a natural hormone’s timing is physiology, not treatment, the same gap our audit of a probiotic sold on GLP-1 claims covers from the supplement side.

The limits are those of any study this demanding: ten healthy adults, one meal of each kind, a lab-made porridge, nobody with diabetes, nothing measured beyond a day. The authors call for larger cohorts, and the 2025 paper named the open question: whether eating intact chickpeas over time improves long-term blood sugar and weight.

What the study does suggest is a kitchen-level idea. A chickpea’s cell walls work as packaging around its starch, as lab work from the same research line has shown, and processing decides whether the packaging survives. Here, long cooking kept cells whole and blending before cooking burst them, and Quadram’s 2025 release notes that making conventional chickpea flour breaks them too. The 2025 authors add that earlier benefits linked to pulses came mostly from whole cooked pulses. Even hummus depends on method: in a 2024 trial of 15 people by overlapping authors, hummus made from intact cells produced lower insulin and GIP responses than hummus from ruptured ones. That does not make smooth foods bad; form is one more variable beside the fiber and protein in our look at two cups of beans a day. If you manage your blood sugar, that is a conversation for your doctor or dietitian. This article is educational, describes what the cited studies report, and is not medical advice.