Study reveals how the structure of food shapes what happens in the gut

Imperial researchers have mapped how the physical structure of food influences what happens inside the human gut, revealing distinct changes in metabolites, microbes and hormones linked to appetite and blood glucose.

The study, led by research in the Department of Metabolism, Digestion and Reproduction and published in Nature Communications, found that chickpea meals with different cellular structures produced different metabolic and microbial environments as they travelled through the gastrointestinal tract. These changes were associated with differences in the release of gut hormones including GLP-1, PYY and GIP.

The findings highlight that food is more than simply a collection of nutrients: how those nutrients are packaged within the structure of food can influence where and when they are released in the gut, and how the body responds to them.

Seeing inside the human gut

The human small intestine is difficult to study directly, meaning much of what is known about how food interacts with the gut has traditionally come from indirect measures, such as stool samples, blood tests or animal studies.

To overcome this challenge, the researchers developed an approach to sample the contents of different regions of the gastrointestinal tract in people.

Working with Dr Dominic Blunt and the imaging team at Charing Cross Hospital, the team used nasoenteric tubes to collect samples from the mouth, stomach, duodenum and ileum following meals. The researchers then analysed the metabolites and microbes present at different stages of digestion, alongside measurements of gut hormone responses.

The randomised crossover study involved 10 participants, who consumed chickpea-based meals with either intact or broken cellular structures.

Food structure changes the body's response

The researchers found that breaking down the cellular structure of the chickpeas changed the timing and location of nutrient release. Meals with broken cellular structures produced earlier increases in glucose and maltose in the gastrointestinal tract, which were associated with more rapid GIP responses.

In contrast, meals with intact cellular structures resulted in higher levels of amino acids in the duodenum and more sugars, amino acids and formate reaching the ileum. These changes were associated with more sustained responses of GLP-1 and PYY – hormones involved in regulating appetite, blood glucose and metabolism.

Dr Mingzhu Cai, Research Associate in Imperial’s Department of Metabolism, Digestion and Reproduction, said: “For the first time, we can see how gut metabolites change as food travels through the human gut and how these changes are linked to GIP, GLP1 and PYY responses. This gives us a powerful foundation for designing foods that support metabolic health.”

The study also revealed changes in the gut microbiome as the meal moved through the digestive system.

The researchers found evidence that bacteria normally found in the mouth travelled with the food to the ileum. The presence of some of these bacteria was associated with local metabolites and PYY responses, suggesting that the food bolus may provide a route for oral bacteria to reach the small intestine and influence its microbial environment.

Towards foods designed for the gut

The researchers say the findings could help develop a better understanding of how the physical structure of foods influences metabolic health.

Rather than considering foods solely in terms of their nutrient content, the findings suggest that the way nutrients are organised within food – and how that structure changes during processing – may also be important.

In the longer term, understanding these mechanisms could help researchers investigate whether foods can be structured to release particular nutrients at specific locations in the gut, potentially supporting appetite regulation and blood-glucose control.
The team’s next step is to establish how these findings could be translated into foods designed to produce specific metabolic responses.