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Preliminary Study Suggests Zinc May Help Diabetics - 11/10/2014
Preliminary Study Suggests Zinc May Help Diabetics
Release Date: November 10, 2014
- Researchers have found that genetic differences may account for why zinc supplements are more beneficial to some people than to others for the prevention and control of diabetes.
- There are more than 50 genetic variants associated with increased risk for type 2 diabetes, and some of these genes or others may also cause people to interact differently with treatments.
- People with diabetes have been known to have more zinc in their urine and less in their bloodstream.
- Previous research also has suggested that higher zinc levels in blood are linked to a lower risk of diabetes.
Researchers at the Johns Hopkins University School of Medicine and elsewhere have found that genetic differences may account for why zinc supplements are more beneficial to some people than to others for the prevention and control of diabetes. The results of their pilot study of a population of Old Order Amish is believed to be the first to point out the relevance of small genetic differences in response to zinc supplementation at play in diabetes management. A report on the work was published last week in Diabetologia.
“There are more than 50 genetic variants associated with increased risk for type 2 diabetes, and some of these genes or others may also cause people to interact differently with treatments,” says Nisa Maruthur, M.D., M.H.S., assistant professor of medicine and epidemiology at the Johns Hopkins University School of Medicine and Bloomberg School of Public Health. “Our results would suggest there are gene-specific differences in how people respond to zinc.” Such knowledge may have wide implications in diabetes management, but more research is needed to show whether that is the case, she says.
People with diabetes have long been known to have more zinc in their urine and less in their bloodstream. And previous research also has suggested that higher zinc levels in blood are linked to a lower risk of diabetes. Adding to the scientific interest in zinc is knowledge of a genetic change affecting one specific protein involved in transporting zinc within cells that secrete insulin. People with the genetic change are more likely to develop type 2 diabetes.
Maruther’s team studied 55 healthy, nondiabetic individuals in Lancaster, Pennsylvania, in an Old Order Amish community, a group that shares a uniform lifestyle and whose genetic background is well understood through detailed genealogy. The researchers analyzed all participants’ DNA sequence for this specific protein alteration. Twenty-three had the alteration, and 32 did not.
Both groups subsequently were given 50 milligrams of elemental zinc twice a day for 14 days — a dose that is similar to zinc supplements available over the counter but also is more than 10 times the recommended daily dietary intake — and their blood sugar and insulin levels were measured five minutes and 10 minutes after an intravenous injection of glucose.
At the end of the two weeks of zinc supplementation, participants without the genetic alteration experienced a 26 percent relative increase in insulin response at five minutes compared to those with the alteration, indicating that zinc may be beneficial to those without the alteration, should they develop diabetes.
Maruthur notes the study population was small, and there was no control group. She says she hopes to conduct a larger study that would look at genetic differences in insulin response and other measures of how the body handles sugar with and without zinc supplementation over a longer period of time, and with a control group. If further research confirms the small study, she notes, zinc supplementation could be an inexpensive treatment to be considered alongside other diabetes medications and lifestyle changes in diet and exercise.
Co-investigators were Jeanne M. Clark and the late Linda Kao of the Welch Center for Prevention, Epidemiology and Clinical Research at the Johns Hopkins University School of Medicine and Bloomberg School of Public Health; and Mao Fu and Alan R. Shuldiner of the University of Maryland School of Medicine.
The research was supported in part by the Mid-Atlantic Nutrition Obesity Research Center (P30 DK072488), the National Institutes of Health, the National Institute of Diabetes and Digestive and Kidney Diseases, and the Johns Hopkins Clinical Research Scholars Program (1KL2 RR025006).