Abstract
Feeding high fat diet (HFD) to mice is a commonly used model to investigate the impact of risk factors on cardiovascular physiology and the development of disease. Therefore, we sought to investigate whether a high fat diet (HFD) alone could produce cardiac dysfunction. Mice were fed a normal chow diet, a milk‐based HFD (60% cal from fat), or a lard‐based HFD (60% cal from fat) for a period of 28 weeks. Neither anesthetized (at 18 weeks) nor conscious echocardiography (28 weeks) revealed any evidence of cardiac dysfunction, despite elevated body fat in the two HFD groups. We next evaluated whether a HFD would exacerbate cardiac dysfunction during heart failure. Mice fed a HFD were subjected to myocardial infarction but experienced no more significant ventricular dysfunction than normal diet fed mice. These largely negative results compelled us to investigate a more severe model of hyperglycemia/obesity. Next, db/db mice were subjected to myocardial ischemia‐reperfusion and demonstrated a significant reduction in fractional shortening compared to wild‐type (WT) littermates. Interestingly, when subjected to pressure overload, db/db mice did not exhibit more severe dysfunction than WT littermates. In conclusion, our findings, coupled with several similar reports from other groups, indicate that a HFD may not reliably replicate the pathophysiological impact of a western diet on the murine heart.Grant Funding Source: Supported by the NIH and AHA
Highlights
Heart disease is the leading cause of death in the United States
We investigated whether long-term feeding of high fat diet alone in naïve mice can cause cardiac dysfunction
After 28 weeks, both the HFDM and HFDL mice weighed significantly more than the low fat diet (LFD) group (51.6±0.5 g and 51.9±0.4 g, vs. 34.3±1.0 g, respectively, p0.05 vs. LFD) and Dexascan analysis showed that the percent fat mass was significantly increased and lean mass was significantly reduced in both the HFDM and HFDL compared to LFD fed mice (Figure 1D-E)
Summary
Heart disease is the leading cause of death in the United States. Over one half of the United States population will be obese by the year 2020. Obesity and diabetes are prominent risk factors for development of heart disease and in order to determine the role these risk factors play in heart disease, various animal models have been employed to recapitulate essential elements of these risk factors. Given the ubiquity of genetically modified mice, many investigators have used diabetic/high-fat fed mouse models to attempt to answer important questions about cardiovascular disease. Some of the most prominent models include leptin receptor deficiency (db/ db), streptozotocin treatment, and high fat diet-induced obesity, all of which were used in the present study
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