Abstract
The involvement of insulin/IGF-1 signals and leptin signals in spinal ligament cells was investigated using Zucker fatty rats (fa/fa) that carry mutation of the leptin receptor gene (fa) and monosodium glutamate-treated (MSG) rats that present obesity due to destruction of the hypothalamic ventromedial nucleus. Zucker fatty rats (ZFR) , that have a with functional abnormality of leptin receptors are a spontaneous model of ossification of the posterior longitudinal ligament that develops sympathetic nerve hypoactivity. (insulin/IGF-1 signals) IRS-1-positive cells, IRS-1 protein were eminent by detected in the cartilage endplate and the enthesis region in ZFR group. On the other hand, IRS-2-positive cells were slightly less in the ZFR group than in the MSG and control groups. The results suggest that IRS-1-mediated signaling for cell proliferation was enhanced in ZFR, which may explain the ossification of the posterior longitudinal ligament. (Leptin signals) We investigated the effects of leptin on the spinal ligament in ZFR histopathologically and immunohistochemically. Since Ob-R does not play any role due to functional abnormality in ZFR, the direct involvement of leptin in ligament ossification may be slight in ZFR. beta(2)AR expression in the stage preceding ligament ossification was confirmed, suggesting that ossification of the spinal ligament may be inhibited by sympathetic nerve stimulation in ZFR.
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