While scientists have known for some time that diets high in fat can trigger a metabolic syndrome—a group of symptoms that represent risk factors for diabetes and heart disease—new research from investigators at Cedars-Sinai Medical Center and Sichuan University in China has revealed that vitamin D deficiency is necessary for this syndrome to progress in mice, which gives hope in the fight against risk factors for diabetes and heart disease. If these new findings can be validated in humans, increased sun exposure and vitamin D supplements may be feasible and affordable options to improve or even prevent metabolic syndrome.
Vitamin D refers to a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, iron, magnesium, phosphate and zinc.
“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,” explained co-senior study investigator Stephen Pandol, Ph.D., director of basic and translation pancreatic research at Cedars-Sinai Medical Center and professor of medicine at UCLA.
The findings from this study were published recently in Frontiers in Physiology in an article entitled “Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models.”
Metabolic syndrome affects nearly one-fourth of the world’s adult population and is defined by a group of risk factors that put sufferers at risk for diabetes and heart disease. Characteristic symptoms include obesity around the waistline and at least two of the following: high blood sugar levels, high blood pressure, or high cholesterol. Moreover, sufferers typically also have excess fat in their liver.
Though the primary cause of metabolic syndrome appears to be a diet high in fat or carbohydrate, observational studies have also linked metabolic syndrome to vitamin D deficiency, which affects 30–60% of the world’s population.
“A sufficient dietary vitamin D supplement can partially, but significantly antagonize metabolic syndrome caused by high-fat diet in mice,” noted Dr. Pandol. “These are amounts equivalent to the dietary recommendations for humans.”
The researchers were able to show that a diet high in fat affected the balance between good and bad bacteria in the gut. This dysbiosis led to modest fatty liver and slightly raised blood sugar levels in mice. Remarkably, the research team found that an insufficient supply of vitamin D aggravated the imbalance in gut flora, contributing to full-scale fatty liver and metabolic syndrome.
The research team noticed that vitamin D deficiency decreased the production of defensins—antimicrobial molecules essential to maintain healthy gut flora. When they supplied mice with an oral dose of a synthetic defensin, the rodents recovered gut bacteria balance, decreased their blood sugar levels, and improved their fatty liver profile.
The researchers did caution against overinterpretation, as the results need to be validated in humans and that work done previously found results that are in contrast to the current study.
“Few studies have indicated that vitamin D supplementation may not improve metabolic disorders in humans,” remarked co-senior study investigator Yuan-Ping Han, Ph.D., professor of biochemistry at Sichuan University. “However, these studies are largely based on long-term surveys, which may be hampered by poor compliance and insufficient dosage.”
Dr. Han remains optimistic that the results of their study will be confirmed in humans and concluded by stating that “we are planning a clinical study to confirm the link between vitamin D deficiency with gut bacteria disruption, and its association with metabolic syndrome.”