This past decade has seen significant advancements in the efficacy of medical procedures, and research on the genetics of type 2 diabetes is one area that has greatly expanded in recent years. As of now, type 2 diabetes is known to be influenced by more than 50 genetic variants, some of which have been studied for their effect on responses to treatment.
Recently published in the journal Diabetologia, a study led by researchers at the Hopkins School of Medicine spearheaded an investigation into a possible link between genetics and insulin response to zinc supplements.
Lead investigator Dr. Nisa Maruthur, an assistant professor of medicine and epidemiology at the School of Medicine and Bloomberg School of Public Health, along with her team, evaluated 55 healthy, non-diabetic individuals of Old Order Amish to better study gene-specific responses to zinc.
Old Order Amish is the term for the most conservative group of Amish people. Maruthur chose them as ideal subjects of the study due to their uniform lifestyles as well as their well-known, detailed genealogy and genetic backgrounds.
To explore genotype-specific insulin response, Maruthur’s team first screened all of the participants’ DNA sequences for a genetic variant affecting a particular protein involved in transporting zinc within beta cells of the pancreas.
The mutated genetic variant coding for the zinc transporter protein was present in 32 of the 55 participants. The other 23 participants possessed the normal form of the gene.
Over a course of 14 days, both groups, with and without the genetic variant, were given 50 milligrams of elemental zinc twice a day, a dosage more than 10 times the recommended daily intake. In addition to the zinc supplement, the participants underwent intravenous glucose injections, after which their blood insulin levels were measured at the initial five- and 10-minute time intervals.
It was discovered that after the glucose injections, the participants with the normal genetic variant demonstrated a 26 percent increase in insulin response at five minutes, whereas participants possessing the mutated variant experienced a lower insulin response at 15 percent at five minutes.
Based on the results of the study, if the participants were diagnosed with diabetes, zinc supplements would be less helpful to the study subjects who displayed a lower insulin response — the individuals with the missense genetic variant. Those possessing the normal variant, however, would most likely benefit more from being prescribed additional zinc supplements.
While this investigation indicates genotype-dependent insulin response to zinc supplements, the study’s limitations and their impact on the results would need to be addressed by improved and expanded studies.
The small size of the sample population as well as the lack of a control group may have potentially skewed the results, and a larger population study would help to reinforce or disprove the conclusion of this study.
Moreover, while one of the strengths of this investigation is the homogeneity of the study population, it is unclear, as Maruthur notes, whether the findings can be reproduced in studies with heterogeneous populations or with patients diagnosed with diabetes.
Nevertheless, the findings of this study hint at the possibility of one day utilizing patients’ genotypes to personalize treatment regimens for type 2 diabetes. Zinc supplements may be an essential addition to the medications and lifestyle changes prescribed for at least some diabetic patients.