Obesity is a worldwide epidemic disease that induces important structural and functional changes to the heart and predisposes a patient to devastating cardiac complications. Sirtuin1 (
SIRT1) has been found to have roles in regulating cardiac function, but whether it can help in cardioprotection is not clear. The aim of the present study was to determine whether
melatonin, by modulating
SIRT1 and in turn mitochondria signaling, may alleviate
obesity-induced cardiac
injuries. We investigated 10 lean control mice and 10
leptin-deficient obese mice (ob/ob) orally supplemented with
melatonin for 8 weeks, as well as equal numbers of age-matched lean and ob/ob mice that did not receive
melatonin. Hearts were evaluated using multiple parameters, including biometric values, morphology,
SIRT1 activity and expression of markers of mitochondria biogenesis, oxidative stress, and
inflammation. We observed that ob/ob mice experienced significant
heart hypertrophy, infiltration by inflammatory cells, reduced
SIRT1 activity, altered mitochondrial signaling and oxidative balance, and overexpression of inflammatory markers. Notably,
melatonin supplementation in ob/ob mice reverted these obesogenic heart alterations.
Melatonin prevented heart remodeling caused by
obesity through
SIRT1 activation, which, together with mitochondrial pathways, reduced oxidative stress and
inflammation.