Abstract
Imidazoline I1-receptors (I1R) are known to regulate blood pressure and rilmenidine, an agonist, is widely used
as antihypertensive agent in clinic. However, the role of I1R in feeding behavior is still unclear. In the present study, we used the agonist
of I1R to investigate the effect on hyperphagia in streptozotocin (STZ)-induced diabetic
mice. Rilmenidine decreased the food intake of STZ-diabetic mice in a dose-dependent
manner. The reduction of food intake was abolished by pretreatment with efaroxan at
the dose sufficient to block I1R. Intracerebroventricular (icv) administration of rilmenidine into STZ-diabetic mice
also significantly reduced hyperphagia, which was reversed by icv administration of
efaroxan. In addition, similar results were observed in STZ-diabetic mice, which received
chronic treatment with rilmenidine 3 times daily (t.i.d.) for 7 days. Moreover, the
hypothalamic neuropeptide Y (NPY) level was reduced by rilmenidine that was also reversed
by pretreatment with efaroxan. In conclusion, the obtained results suggest that rilmenidine
can decrease food intake in STZ-diabetic mice through an activation of I1R to lower hypothalamic NPY level.
Key words
feeding - hyperphagia - imidazoline I
1-receptors - neuropeptide Y - STZ-diabetic mice