These findings are being presented for the first time at the 2011 Experimental Biology Meeting sponsored by the American Society for Pharmacology and Experimental Therapeutics on April 13 in Washington, D.C.
Lauren Haar, a doctoral student in the Systems Biology and Physiology Graduate Program, found that short-term, high-fat feeding in animal models led to cardioprotection against myocardial infarction (MI, or heart attack) and resulted in less cardiac tissue damage.
“Previous clinical studies have supported the idea that certain patients with high serum cholesterol levels have better survival rates when their heart fails after cardiac ischemic injury than those with lower cholesterol levels, but the reason for this is unclear,” she says. “Previous research using a heart failure animal model paired with chronic high-fat feeding showed improvement in heart function and modulation of cardioprotective gene profiles. However, there are very few studies geared toward understanding the acute effect of these diets on MI.
“We wanted to see if the same was true in models of acute high-fat feeding paired with simulated heart attacks.”
For the study, researchers fed one group of mice a high-fat diet (60 percent of the calories coming from saturated fat) for two weeks or less. A second group received the high-fat diet for six weeks, and a control group received a regular, grain- and vegetable-based diet.
“We then induced heart attack in all groups and assessed the cardiac function and extent of injury to the tissue,” Haar says. “Our results showed that injury in mice fed a high-fat diet acutely (two weeks or less) was reduced by 70 percent when compared to the groups fed on a high-fat diet for six weeks or fed on a control grain and vegetable based diet.”
She says that there was no cardioprotection observed in the six-week group, indicating that short-term splurges are key, and the effects of sustained high-fat feeding, including obesity and diabetes, do not contribute to cardioprotection.
“In addition, animals fed a high-fat diet for 24 hours and then returned to a control diet for 24 hours prior to heart attack experienced a prolonged or ‘late phase’ protection against injury,” she adds. “This shows that acute—or short-term—high-fat feeding in animal models does preserve cardiac function.”
Haar says more studies are in the works to find the factors that initiate this response in the body.
“This could mean great things for patient care if we can find the mechanisms that come into play to cause this cardioprotection,” she says, adding that this could be a way to “pre-treat” patients at risk of heart attack. “This also may show that, while it’s important to eat right, not all ‘bad’ foods—like red meat—should be avoided all of the time. This could change the way we view nutrition and dietary recommendations.”
Haar conducted her research under the direction of Keith Jones, PhD, associate professor in the department of pharmacology and cell biophysics, and Jack Rubinstein, MD, assistant professor of medicine in the division of cardiovascular diseases and UC Health cardiologist.
This study was funded by the National Institutes of Health and a UC Rehn award. Rehn Family Research awards are internal grants that support the research development of internal medicine junior faculty, clinical and postdoctoral fellows, residents, graduate students and medical students.