New research from the Oklahoma Medical Research Foundation has pinpointed a cellular switch linked to why diabetes negatively affects the heart.
The findings could lead to new treatments to limit the damaging cardiac effects of diabetes, said OMRF researcher Kenneth Humphries, Ph.D., who led the study.
A healthy heart has the ability to respond and adapt in order to use available nutrients—either fat or sugar—for energy. However, diabetes disrupts the heart’s ability to be flexible in this way. This disruption can ultimately result in a number of heart problems for diabetics.
Heart problems are the leading cause of death in people with diabetes. According a study in the journal Diabetologia, people with diabetes—both type 1 and type 2—are more than twice as likely the general population to die from heart disease or stroke.
In the new study, Humphries and his OMRF team discovered that a particular cellular protein (called PFK-2), which is known to be critical for allowing the heart to use sugar properly, is broken in a diabetic heart.
“This is important because the heart normally uses fat for energy, but it needs to maintain its flexibility to use sugar when your insulin levels rise, like after a meal,” said Humphries. “When your heart loses this flexibility, it helps explain why heart problems eventually develop.”
Diabetics have trouble producing or responding to insulin, a hormone that tells cells to take in sugar as a source of energy. Long-term effects of the illness, which impacts more than 29 million Americans, include heart disease and other cardiovascular conditions.
Humphries said understanding the role of PFK-2 could allow researchers to develop therapies to regulate this important protein, restoring the heart’s normal functions even in a diabetic setting.
“We are excited because we think if we can activate or help this broken switch, it might keep the heart more flexible, which would diminish some of the effects diabetes has on the heart and potentially reduce the likelihood of developing life-threatening heart conditions,” said Humphries.
The research was published in the Journal of the American Heart Association. Other OMRF researchers who contributed to the findings were Satoshi Matsuzaki, Ph.D., Zack Young, Jennifer Giorgione, Ph.D., Maria Newhardt, Mike Kinter, Ph.D., and Lee Bockus, Ph.D.
Funding for this research was provided by grant Nos. 1R01HL125625 from the National Heart, Lung, and Blood Institute, P30AG050911 from the National Institute on Aging, and P20GM104934 from the National Institute of General Medical Sciences. All three of these are a part of the National Institutes of Health.