Extra Vitamin D can restore good bacteria in the gut, according to a study on mice, giving hope in the fight against risk factors for diabetes and heart disease.
Scientists have now discovered that Vitamin D deficiency is necessary for this syndrome to progress in mice, with underlying disturbances in gut bacteria.
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The study, published in the journal Frontiers in Physiology, found that an insufficient supply of Vitamin D aggravates the imbalance in gut flora, contributing to full-scale fatty liver and metabolic syndrome.
If these findings can be validated in humans, sun bathing and Vitamin D supplements may be feasible and affordable approaches to improve or even prevent metabolic syndrome.
“Based on this study, we believe that keeping Vitamin D levels high, either through sun exposure, diet or supplementation, is beneficial for prevention and treatment of metabolic syndrome,” said Professor Stephen Pandol from Cedars-Sinai Medical Centre in the US.
The main cause of metabolic syndrome appears to be a diet high in fat or carbohydrate.
However, observational studies have also linked metabolic syndrome to Vitamin D deficiency, which affects 30 to 60 percent of the world’s population.
The research team made important advances in understanding the causative role of Vitamin D in this syndrome.
“A sufficient dietary Vitamin D supplement can partially but significantly antagonise metabolic syndrome caused by high fat diet in mice,” says Pandol
“These are amounts equivalent to the dietary recommendations for humans.”
More specifically, they have shown that a high fat diet affects the balance between good and bad bacteria in the gut. This induces modest fatty liver and slightly raises blood sugar levels in mice.
Vitamin D deficiency decreases the production of defensins, which are anti-microbial molecules essential to maintain healthy gut flora. As expected, an oral supply of a synthetic defensin recovers gut bacteria balance, decreases blood sugar levels and improves fatty liver.
Accordingly, Vitamin D supplementation improves metabolic syndrome in mice. The next step would be to validate the results in humans.
