April 14, 2009
Researcher finds damaged binding proteins could be key contributor to diabetics’ poor vitamin D absorption
Rowling’s NWRC-funded study isolates the likely cause of type 2 diabetics’ disrupted metabolism of the important vitamin
Matthew Rowling, professor in food science and human nutrition and a scientist in the Nutrition and Wellness Research Center, studies type 2 diabetics’ metabolism of vitamin D in order to determine how to best reduce their risk of developing negative effects associated with the disease. |
By
Steve Adams
“Nutrition is something that every human being is exposed to, so what better vehicle can be used to reduce the incidence of chronic disease,” said Matt Rowling, assistant professor in food science and human nutrition and a scientist in the Nutrition and Wellness Research Center.
Rowling, who joined the faculty in 2008, is already proving this commitment to enhancing human wellness through nutrition.
Rowling is studying diabetics’ metabolism of nutrients to determine how to best reduce their risk of developing negative effects of the disease.
In his most recent study – one of ten projects funded through the NWRC’s $450,000 grant awarded by the United States Department of Agriculture last October – Rowling explored type 2 diabetics’ metabolism of vitamin D and resulting levels of the nutrient. Rowling says that he was interested in vitamin D because vitamin D deficiency is known to play a role in the development of a number of chronic diseases – particularly colon and breast cancer – which type 2 diabetics are diagnosed with at a disproportionately high rate.
Rowling explains that the kidney, where vitamin D is processed, is composed of cells that contain a complex of receptor proteins – cubilin, megalin, and dab-2. Attached to a binding protein, vitamin D circulates, enters the kidney, and either reenters the blood stream or gets flushed out in urine.
In his study, Rowling found that diabetic rats lost much more vitamin D in their urine than did non-diabetic rats. He also found that two of the binding proteins necessary for the functioning of megalin and dab-2 were significantly reduced in the diabetic rats. While this finding represents a correlation and has not yet been proven as a conclusive cause, Rowling says that it likely explains at least part of why vitamin D absorption is disrupted in diabetics.
“These proteins are needed to keep vitamin D status at an optimum level,” Rowling said. “So far, we think that the more kidney damage diabetics have, the higher their vitamin D requirements will be. These findings will help outline the requirement of vitamin D for a diabetic – particularly a type 2 diabetic, which is important because the incidence [of that type] is increasing so dramatically.”
Of the nearly 25 million Americans who have diabetes, roughly 90 percent have the type 2 form of the disease. Over 57 million more Americans are at a high risk of developing type 2 diabetes.
To help stem these risks, Rowling continues to research the disease. Moving forward, he is now working to determine what level – if any – of vitamin D supplement might normalize the metabolic abnormalities of a type 2 diabetic.
“The hope is that maybe we can come up with a cheap, safe, and practical strategy to modify the expression of these proteins which are necessary for vitamin D re-absorption,” Rowling said.
A simple increase in vitamin D intake might be all that is needed. If so, Rowling is confident that type 2 diabetics will be able to combat at least one of the many factors that contribute to their disproportionate development of life-threatening diseases.
