In a new study, Penn State researchers revealed that broccoli has unique compounds that attach to a receptor in mice and help to protect the lining of the small intestine, delaying the start of sickness. The findings show that broccoli is a "superfood" in the truest sense. The results of the investigation were published in the journal Laboratory Investigation.
"We all know broccoli is good for us, but why is that?" "What happens inside our bodies when we eat broccoli?" Penn State's Gary Perdew is the H. Thomas and Dorothy Willits Hallowell Chair in Agricultural Sciences. "Our research is assisting in the discovery of the mechanisms by which broccoli and other foods benefit health in mice and, most likely, humans."
It presents compelling evidence that cruciferous vegetables including broccoli, cabbage, and Brussels sprouts should be included in a healthy diet. According to Perdew, the small intestinal wall permits helpful water and nutrients to enter the body while blocking harmful food particles and bacteria.
Enterocytes, which absorb water and nutrients; goblet cells, which secrete a protective layer of mucus on the intestinal wall; and Paneth cells, which secrete lysosomes containing digestive enzymes — all help to modulate this activity and maintain a healthy balance. Perdew and his colleagues discovered that chemicals in broccoli known as aryl hydrocarbon receptor ligands bind to the aryl hydrocarbon receptor (AHR), which is a type of protein known as a transcription factor.
They discovered that this binding triggers a number of processes that impact the functionality of intestinal cells. The researchers offered an experimental group of mice a diet containing 15% broccoli- comparable to around 3.5 cups per day for people- 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, as well as the amounts of different cell types and mucus concentrations, among other things, in the two groups.
The researchers discovered that mice that were not fed broccoli lacked AHR activity, which resulted in altered intestinal barrier function, decreased food transit time in the small intestine, a decrease in the number of goblet cells and protective mucus, a decrease in Paneth cells and lysosome production, and a decrease in the number of enterocyte cells.
"The gut health of the mice not fed broccoli was compromised in a variety of ways that are known to be associated with disease," Perdew explained. "Our findings suggest that broccoli, and possibly other foods, can be used as natural sources of AHR ligands, and that diets high in these ligands contribute to small intestine resilience." "These data suggest that dietary cues, relayed through the activity of AHR, can reshape the cellular and metabolic repertoire of the gastrointestinal tract," said Andrew Patterson, John T. and Paige S. Smith Professor of Molecular Toxicology and Biochemistry and Molecular Biology.
(Source: Penn State)
