It is well known that broccoli is good for human health. For instance, studies have indicated that increasing the intake of cruciferous vegetables lowers the risk of type 2 diabetes and cancer.
Researchers at Penn State discovered in a new study that broccoli has particular molecules that attach to a receptor in mice and help to preserve the lining of the small intestine, preventing the onset of disease. The study confirms that broccoli is a “superfood,” as suggested.
We all know that broccoli is good for us, but why? What happens in the body when we eat broccoli? Our research is helping to uncover the mechanisms for how broccoli and other foods benefit health in mice and likely humans, as well. It provides strong evidence that cruciferous vegetables, such as broccoli, cabbage, and Brussels sprouts should be part of a normal healthy diet.”
Gary Perdew, H. Thomas and Dorothy Willits Hallowell Chair, Agricultural Sciences, Pennsylvania State University
According to Perdew, the small intestine’s wall stops infectious bacteria and food particles from entering the body while permitting healthy water and nutrients to do so.
A few intestinal lining cells, such as enterocytes, which absorb nutrients and water, goblet cells, which secrete a layer of protective mucus on the intestinal wall, and Paneth cells, which release lysosomes containing digestive enzymes, assist in controlling this activity and maintaining a healthy balance.
Perdew and his colleagues discovered in their study, which was published in the journal Laboratory Investigation, that molecules in broccoli known as aryl hydrocarbon receptor ligands bind to aryl hydrocarbon receptor (AHR), a type of protein known as a transcription factor. They discovered that this binding starts several processes that have an impact on how cells in the intestine operate.
The researchers offered an experimental group of mice a meal containing 15% broccoli—similar to around 3.5 cups per day for humans—and a control group of mice a standard lab diet that did not contain broccoli.
They next examined the tissues of the animals to see how much AHR was activated, in addition to the amounts of different cell types and mucus concentrations, among other things, in the two groups.
The researchers discovered that mice lacking AHR activity had altered intestinal barrier function, a shorter time for food to pass through the small intestine, fewer goblet cells and protective mucus, fewer Paneth cells and lysosome production, and fewer enterocyte cells.
Perdew added, “The gut health of the mice that were not fed broccoli was compromised in a variety of ways that are known to be associated with disease. Our research suggests that broccoli and likely other foods can be used as natural sources of AHR ligands, and that diets rich in these ligands contribute to resilience of the small intestine.”
Andrew Patterson, John T. and Paige S. Smith Professor of Molecular Toxicology and of Biochemistry and Molecular Biology, further stated, “These data suggest that dietary cues, relayed through the activity of AHR, can reshape the cellular and metabolic repertoire of the gastrointestinal tract.”
Zhou, X., et al. (2023). Aryl Hydrocarbon Receptor Activation Coordinates Mouse Small Intestinal Epithelial Cell Programming. Laboratory Investigation. doi.org/10.1016/j.labinv.2022.100012