Gut microbes may link with a protein to help regulate vitamin D

A collection of bacteria in the gut may use a cell-signaling protein to help regulate vitamin D.

"The changes in the microbiota might affect how much vitamin D a person can metabolize, or how the body metabolizes vitamin D, so there are implications, but it's still early and that remains to be seen," said Cantorna. Image: © iStock Photo / royaltystockphoto

An accumulation of bacteria in the gut may utilize a cell signaling protein to help manage vitamin D, a key supplement that, among different advantages, is included with building and maintaining bones, as indicated by a group of analysts.

In an examination on mice, specialists found that microbiota — a network of microorganisms in the gut that can help digest food and maintain the immune system— may regulate the metabolism of endocrine vitamin D through a protein called fibroblast development factor 23, or FGF 23. FGF 23 is a protein that sends signals to activate receptors located on the outside surface of cells.

Margherita T. Cantorna, distinguished professor of molecular immunology in Penn State’s College of Agricultural Sciences said, “It has been known that the amount of vitamin D in the gut can influence the microbiota.”

“When you don’t have enough vitamin D, the types of microbes in your gut change. Before we did this work, we started to think that this might be a two-way street and that the microbiota may also have an effect on how much vitamin D you had available and how it was utilized by a person.”

Scientists conducted a study on germ-free mice and then measured the levels of different types of vitamin D at different times as the researchers introduced microbes into their systems during a two-week period.

The germ-free mice started with low levels of three kinds of vitamin D — 25hydroxy vitamin D, 24,25 dihydroxy vitamin D, and 1,25 dihydroxy vitamin D — and with low levels of calcium and large amounts of FGF 23 in the bloodstream. After the microbiota was introduced, the mice continuously achieved normal vitamin D and calcium levels. The scientists likewise watched an underlying drop in FGF 23 levels before vitamin D standardized.

The length of time it took to re-establish vitamin D levels indicated that regulation was an indirect, multi-step process. It suggests that the microbiota does not work directly on increasing vitamin D levels, but instead may be inducing inflammation, which shuts off FGF23 and, in turn, causes a rise in vitamin D levels.

Cantorna said, “The amount of vitamin D that you make in your skin with sunshine exposure is extremely variable. Obviously, you have to go out in the sun, so in some seasons you might not make any; darker skin makes less; and you make less as you age, so it’s very difficult to regulate how much you’re making in your skin. And there’s also skin cancer. Really, for most people, the best way to get vitamin D is to eat it, or eat foods that are fortified with vitamin D.”

“this is only a preliminary step and a lot of work must be completed before researchers can say conclusively whether the findings on the microbiota and vitamin D may apply to humans.”

“The changes in the microbiota might affect how much vitamin D a person can metabolize, or how the body metabolizes vitamin D, so there are implications, but it’s still early and that remains to be seen.”

The authors of the study includes Stephanie A. Bora, former doctoral fellow at Penn State and currently post-doctoral research fellow in the Lung Institute, Cedars-Sinai Medical Centre, and Mary J. Kennett, professor of veterinary and biomedical sciences and director of the animal resource program; Philip B. Smith, director, metabolomics core facility and senior research associate, proteomics and mass spectrometry core facility, Huck Institutes of the Life Sciences and Andrew Patterson, associate professor of molecular toxicology and associate professor of biochemistry and molecular biology, all of Penn State.

Scientists reported their study in a recent issue of Frontiers in Immunology.