Key result
Aged mice fed a high-fat diet developed overt heart failure with a reduced ejection fraction of 41.4% and impaired physical performance, whereas young mice were protected from cardiac dysfunction.
Why the study?
The maladaptive cardiac responses resulting from prolonged obesity and the specific impact of biological age remained incompletely understood.
Does a high-fat diet induce cardiac dysfunction and impair physical performance differently in aged versus young male mice?
Does a high-fat diet induce cardiac dysfunction and impair physical performance differently in aged versus young male mice?
Diet-induced obesity in aged mice leads to a heart failure phenotype and impaired physical performance, whereas young mice exhibit proteomic adaptations that protect against cardiac dysfunction.
This animal model of diet-induced HFrEF should not yet change clinical practice; leaves open whether.
Aging in the context of obesity exacerbates the risk of morbidity and mortality related to cardiovascular disease. However, the maladaptive responses in the heart that arise from prolonged obesity and the specific influence of biological age remain somewhat elusive. This study investigated the effects of diet-induced obesity (DIO) and aging on physical performance and cardiovascular function in mice. 22- and 76-week-old male C57BL/6J mice were randomized to 8 weeks of chow or high-fat diet. Body weight was assessed weekly. Body composition was measured at the beginning and the end of the diet treatment. Muscular and cardiac function were evaluated at the end intervention. Aged mice with DIO exhibited faster and greater body weight gain and fat mass accumulation, reduced running distance, and lower aerobic capacity. Aged HFD mice also exhibited increased cardiac lipid accumulation and cardiomyocyte hypertrophy, with no major morphological changes observed in skeletal muscle. Proteomic analysis revealed differential expression of heart proteins associated with metabolic function in young mice, which was not observed in aged mice with DIO. Subsequently, aged mice with DIO developed overt heart failure with reduced ejection fraction, while cardiac function was unaffected by DIO in young mice. In conclusion, young mice with DIO were protected against diet-induced cardiac dysfunction, whereas DIO in aged mice led to heart failure and impaired physical performance. The protective effects observed in younger mice appear to be explained by proteomic-level remodeling of the heart oriented to sustain cardiac function.
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Kamp et al. (2025) studied Diet-induced obesity and aging. High-fat diet vs. Chow diet was evaluated on Cardiac function (ejection fraction). Aged mice fed a high-fat diet developed overt heart failure with a reduced ejection fraction of 41.4% and impaired physical performance, whereas young mice were protected from cardiac dysfunction.
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