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Obesity is an independent risk factor for heart diseases but the underlying mechanism is not clear. This study examined cardiac contraction, oxidative stress, oxidative modification of sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA) and the myosin heavy chain (MHC) isoform switch in obese mice.

Mechanical properties were evaluated in ventricular myocytes from C57BL/6J lean and Lep/Lep obese mice (formerly known as ob/ob mice), including peak shortening (PS), time to 50 or 90% PS, time to 50 or 90% relengthening (TR₅₀, TR₉₀), maximal velocity of shortening/relengthening (±dL/dt), intracellular Ca²⁺ and its decay (τ). Oxidative stress, lipid peroxidation, protein damage and SERCA activity were assessed by glutathione/glutathione disulfide, malondialdehyde, protein carbonyl and ⁴⁵Ca²⁺ uptake, respectively …