Leptin blocks the fasting-induced increase of pERK1/2 in the paraventricular nucleus of rats.

摘要

This study was conducted to define molecular mechanisms by which food deprivation increases phosphorylated extracellular signal-regulated protein kinase (pERK1/2) in the hypothalamic paraventricular nucleus of rats. pERK1/2 immunoreactivity (-ir) is markedly increased in the paraventricular nucleus by 48h of food deprivation. Treatment with RU486, glucocorticoid antagonists, during food deprivation did not affect the fasting-induced increase of pERK1/2-ir in the paraventricular nucleus, but intracerebroventricular (icv) leptin blocked the increase of pERK1/2-ir by food deprivation. Fasting-induced increases of neuropeptide Y (NPY) expression both in the arcuate nucleus and the paraventricular nucleus were also blunted by icv leptin; however, the icv NPY to satiated rats did not increase pERK1/2 in the paraventricular nucleus. These results suggest that the fasting-induced increase of pERK1/2 in the paraventricular nucleus may not be mediated either by plasma corticosterone or the hypothalamic NPY, but require leptin dis-inhibition.