Effects on food intake following stimulation of alpha1- and alpha2-adrenoceptors within the hypothalamic paraventricular nucleus of dietary-obese and dietary-resistant rats

Abstract

Rats fed diets high in fat and sucrose exhibit varying degrees of obesity. Studies have sought to define differences between dietary-obese (DIO) rats and dietary-resistant (DR) rats which may contribute to the cause or development of obesity. Adrenergic receptor activity is altered in dietary obesity with DIO rats exhibiting reduced numbers of (x2adrenoceptors in brain prior to obesity yet reduced numbers of (xl-adrenoceptors after the development of obesity. Adrenergic receptors within the paraventricular hypothalamic nucleus (PVN) modulate feeding: activation of PVN (x2-adrenoceptors stimulates feeding whereas activation of PVN (xl-adrenoceptors suppress feeding. Experiment 1 of the present study investigates food intake of DIO and DR rats (post-obesity) following intra-PVN injections of the adrenergic compounds norepinephrine (25 nmol), cirazoline (10, 20, and 30 nmol), and phenylpropanolamine (160 nmol) . Experiment 2 investigates food intake of DIO-prone and DR-prone rats (pre-obesity) following intra-PVN injections of norepinephrine (10, 20, and 30 nmol) and phenylpropanolamine (80, 160, and 240 nmol) . Experiments I and 2 found no differences in adrenergic functioning between dietary-obese and dietary-resistant rats either before or during obesity. Experiment 2 revealed that there was a difference in the dose-response of norepinephrine(10, 20, and 30 nmol) elicited feeding between DIO-and DRprone rats. Another difference between DIO and DR rats has been identified by Levin (1994) who noted a correlation between degree of dietary-obesity and urinary norepinephrine (NE) level in rats with DIO-prone rats exhibiting greater urinary NE levels than DR-prone rats. This relationship was investigated in Experiment 2 and the absence of a significant correlation between weight gain and urinary NE level was obtained.