High saturated fat feeding in a rat model of heart failure improved in vivo myocardial contractile function and prevented myosin heavy chain isoform switching, without altering Ca2+ regulation.
Does a high saturated fat diet improve contractile function and alter myofilament protein expression in a rat model of heart failure?
A high saturated fat diet improves contractile function in a rat model of heart failure by altering myofilament function rather than sarcoplasmic reticulum Ca2+ regulation.
Pathological conditions such as diabetes, insulin resistance, and obesity are characterized by elevated plasma and myocardial lipid levels and have been reported to exacerbate the progression of heart failure (HF). Alterations in cardiomyocyte Ca 2+ regulatory properties and myofilament proteins have also been implicated in contractile dysfunction in HF. However, our prior studies reported that high saturated fat (SAT) feeding improves in vivo myocardial contractile function, thereby exerting a cardioprotective effect in HF. Therefore, we hypothesized that SAT feeding improves contractile function by altering Ca 2+ regulatory properties and myofilament protein expression in HF. Male Wistar rats underwent coronary artery ligation (HF) or sham surgery (SH) and were fed normal chow (SHNC and HFNC groups) or a SAT diet (SHSAT and HFSAT groups) for 8 wk. Contractile properties were measured in vivo echocardiography and left ventricular (LV) cannulation and in isolated LV cardiomyocytes. In vivo measures of contractility (peak LV +dP/d t and −dP/d t) were depressed in the HFNC versus SHNC group but improved in the HFSAT group. Isolated cardiomyocytes from both HF groups were hypertrophied and had decreased percent cell shortening and a prolonged time to half-decay of the Ca 2+ transient versus the SH group; however, SAT feeding reduced in vivo myocyte hypertrophy in the HFSAT group only. The peak velocity of cell shortening was reduced in the HFNC group but not the HFSAT group and was positively correlated with in vivo contractile function (peak LV +dP/d t). The HFNC group demonstrated a myosin heavy chain (MHC) isoform switch from fast MHC-α to slow MHC-β, which was prevented in the HFSAT group. Alterations in Ca 2+ transients, L-type Ca 2+ currents, and protein expression of sarco(endo)plasmic reticulum Ca 2+ -ATPase and phosphorylated phospholamban could not account for the changes in the in vivo contractile properties. In conclusion, the cardioprotective effects associated with SAT feeding in HF may occur at the level of the isolated cardiomyocyte, specifically involving changes in myofilament function but not sarcoplasmic reticulum Ca 2+ regulatory properties.
Cheng et al. (2011) studied Heart failure. High saturated fat (SAT) diet vs. Normal chow was evaluated on In vivo measures of contractility (peak LV +dP/dt and -dP/dt) and isolated cardiomyocyte properties. High saturated fat feeding in a rat model of heart failure improved in vivo myocardial contractile function and prevented myosin heavy chain isoform switching, without altering Ca2+ regulation.