Concentrations of
leptin, an adipocyte-derived
hormone, are elevated in
obesity. Recently,
leptin has been shown to participate in multiple biological actions including
inflammation, reproduction, and angiogenesis.
Leptin has also been documented as a critical component in the process of wound healing; however,
leptin involvement in
cardiovascular disease is poorly understood. We examined the expression of
leptin (ob) and
leptin receptor (ob-R) genes in the rat heart following
ischemia/reperfusion, which was induced by coronary artery
ligation, and
mRNA was obtained from hearts 0.5 to 36 h after initiating reperfusion. Expressions of ob and ob-R
mRNA were examined by real-time quantitative RT-PCR and immunohistochemistry. The ob and ob-Ra
mRNA and
protein expressions were significantly increased (p<0.01) and ob-Rb
mRNA was significantly decreased (p<0.01) in hearts after 8 h of reperfusion. Furthermore, ob and ob-R
proteins were expressed in injured myocytes where inflammatory cells infiltrated. In contrast, those expressions were not influenced in hearts after 8 h of
ischemia stress only. To determine the functional effects of
leptin on the ischemic/reperfused heart, rats were treated with anti-
leptin antibodies prior to
ischemia/reperfusion; however, this treatment did not affect the elevation of
mRNA expression levels of inflammatory markers such as
TNF-alpha and IL-1beta in ischemic hearts. Our results demonstrated for the first time that
ischemia/reperfusion induced
leptin and
leptin receptor gene expression in the rat heart. This study helps to elucidate the mechanisms behind the onset and development of
ischemic heart disease concomitant with
obesity.