Effects of Repeated Restraint Stress on Tissue Metabolism in Rats.

It has been reported that repeated restraint stress (RS), 3 hours/day for 3 days, in rats caused sustained weight loss and a temporary drop in daily food intake with no subsequent compensatory overeating during the post stress period. The hypothesis tested in the present study is that RS causes peripheral tissue metabolism changes which account for the abnormal regulation of body weight and food intake during the post stress period. Adult male Sprague Dawley rats were assigned to control, pair fed (PF) or RS groups. One day after the end of RS, midbrain urocortin mRNA was at control levels in RS rats, but elevated in PF rats. NPY content in hypothalamus PVN was the same for all groups, These results confirm that the acute effects of stress were already reversed one day after stress. The initial weight loss during stress was lean tissue, but 5 days post-stress, it was both lean and fat. In an oral glucose tolerance test one day after RS, insulin release was blunted but glucose clearance was normal. A number of measurements for lipid and glucose metabolism were made in peripheral tissues. The major differences in RS rats were a substantial inhibition of adipocyte, but not muscle, glucose transport. In contrast, adipocyte fatty acid oxidation was increased. In the liver, there was an increment of hepatocyte glucose transport in RS rats. This extra glucose was stored as a glycogen in the liver. beta-adrenergic receptor number was increased in adipose but not in liver from RS rats, which implies that lipolysis was increased in RS rats. These results demonstrate that RS affected nutrient partitioning and specific tissue nutrient metabolism during the post stress period. The increased glucose uptake and storage in liver may contribute to the absence of compensatory hyperphagia in stressed animals. The switch from glucose to fatty acid utilization in adipocytes may account for the post stress change in body composition and the sustained weight loss in RS rats. As beta-adrenergic receptor number was increased in adipose tissue, this may be responsible for the changes in adipose metabolism